Sunday 14 February 2016
Microbes Vs.Darwin II
More on How Microbes Make Earth Habitable:
Evolution News & Views February 14, 2016 12:03 AM
Last week we discussed how microbes maintain the viability of life on our planet ("How Microbes Make Earth Habitable"). In the same vein, more news just arrived about the carbon and nitrogen cycles.
Following up on MIT's findings about plankton taking carbon to the ocean bottom, Ohio State has just concluded from the three-year Tara Oceans oceanography expedition that plankton -- and some viruses -- are "key to carrying carbon" from the atmosphere down to the seafloor sediments. They took pictures of microbes at different depths to learn which ones are carrying carbon downward as they sink to the bottom. The research has helped scientists understand "the interplay of organisms in the ocean and of their role in the health of the planet."
As for nitrogen, Current Biology posted a Primer on "The Nitrogen Cycle," confirming that it "is entirely controlled by microbial activities." Before man started producing chemical fertilizers, "nearly all of the reactive nitrogen in the biosphere was generated and recycled by microorganisms."
Microbes Follow Icebergs
Another interesting interaction between geology and life was reported by the BBC News. Mark Kinver writes that "Giant icebergs play [a] 'major role' in [the] ocean carbon cycle." An aerial image shows a brilliant bloom of phytoplankton following one such giant iceberg in its wake. What's happening? The bloom is "triggered by the distribution of nutrients -- such as iron -- from an iceberg's meltwater." What this signifies is important:
"We estimate that giant icebergs account for between 10% and 20% of the actual vertical rate of carbon going from the surface to the deep (Southern) Ocean," he suggested....
Plankton scientist Dr Richard Kirby, who was not involved in this study, observed: "The phytoplankton at the sunlit surface of the sea has played a central role in the sequestration of carbon over millennia to affect the atmospheric concentration of this greenhouse gas, and so the Earth's climate.
"This interesting paper shows how much we still have to learn about these microscopic organisms, and how a changing climate may affect them, and also the food web they support." [Emphasis added.]
Bacteria Attack Lignin
Readers of Evolution News may remember Ann Gauger and Matt Leisola's design inference about lignin, the complex molecule that gives wood its strength. They argued that no organism has exploited this energy-rich substance -- which is good news for us, because "the indigestibility of lignin may be an essential requirement for the balance of life," Gauger wrote. "Lignin slows the degradation of wood, thus allowing the buildup of humus in the soil, which in turn permits plant growth and all resulting life that depends on plants."
Now, news from Rice University says that bacteria use a "tag team" approach to break apart this complex substance that locks up more than half a plant's sugar and holds a third of the carbon in biomass. This finding does not impact the conclusions of Gauger and Leisola, because the bacteria "chew through" the lignin to get to the cellulose they can digest. But "it's a very slow process, which is why it can take years for dead trees to decompose." The rate of decomposition of this energy-rich substance is what's interesting for considerations of planetary carbon cycling and habitability.
Bacteria Prepare the Land for Habitation
Another interesting interaction of microbes with geology happens on land. Biocrusts are accumulations of cryptic bacteria that inhabit the surfaces of arid soils. A paper in Nature Communications notes the ecological impact of these microbial habitats:
Much of the arid soil surfaces can be populated by cryptic photosynthetic assemblages known as biological soil crusts (or biocrusts), which are known to impart stability against erosion, to modify the hydrological properties of soils, and to contribute significantly to arid land fertility.
Researchers from Arizona and California found that the bacteria, mostly the nitrogen-fixing variety, produce a secondary metabolite called scytonemin that acts as a "sunscreen". It strongly absorbs solar radiation and dissipates it as heat, raising soil temperatures as much as 10°C, an effect that is "not without consequences" for soil microbial communities. While potentially making deserts more arid, this effect is good for temperate and arctic zones: "biocrusts in cold climates, that is, in polar settings or during winter months when activity is limited by temperature, the warming can be expected to be largely beneficial to biological entities."
About 41 percent of the earth's surface is arid, and this is where biocrusts figure prominently. By producing this sunscreen molecule, bacteria protect the soil from harmful radiation while simultaneously raising the temperature in cold arid lands to promote the growth of complex plants in ecological succession -- all this while stabilizing the soil, reducing erosion and fixing nitrogen that higher plants need. It's another case that has just come to light of global benefit from the world's smallest organisms.
For these reasons, microbial effects on land surface albedo may have global scale repercussions historically and in the present, and should be evaluated in models of planetary radiation budgets as a new twist of biosphere-climate feedback interactions. This may shed some light into the apparent inconsistency in temperature changes recorded in arid lands. Contrary to model predictions, temperature has been shown to increase when removing vegetation there, an apparent paradox that could potentially be explained by biocrust colonization. Based on estimates of the global biomass of cyanobacteria in soil biocrusts, one can easily calculate that there must currently exist about 15 million metric tons of scytonemin at work, warming soil surfaces worldwide.
Big Animals Help Earth's Habitability, Too
From orbit, a bear would appear as small as a microbe. Current Biology published another indication that all living things, even the big ones, have a stake in keeping the earth habitable. In "Megafauna move nutrients uphill," Michael Gross points to research about whales, salmon, birds and bears that reveal large animals' roles in moving phosphorus and nitrogenous compounds from the deep ocean to the mountains. These "ecosystem engineers" perform an "important ecosystem service" by distributing nutrients to higher elevations.
Given the laws of gravity and the hydrological cycle, there is a strong likelihood that nutrients available on land, even though they may go through many cycles around the food web, will eventually be washed out to the sea. In the oceans, there is the risk that they will drop out of the photic zone and reach the sea floor, where they will be buried in sediment that may only be returned to circulation on geological timescales, some tens or hundreds of millions of years later.
Animals can make important contributions to stem this flow, as was first reported for whales back in 2010 (Curr. Biol. (2010) 20, R541). Researchers studying the ecology of sperm whales found that they harvest nutrients such as iron from great depths (often more than 1,000 metres), where they hunt cephalopods, but release them when they defecate near the surface.
The nutrients are incorporated into microbes, plankton, and fish that become prey for birds and mammals. These larger animals, in turn, transport the nutrients up rivers and mountains. Although Michael Gross focuses on how humans are disrupting this natural system, one can only stand in awe of how the living web distributes the very atoms and molecules needed for complex life around the globe.
Tiny Creatures, Major Roles
It takes more than a rocky planet in a habitable zone to sustain life. Some twenty factors are listed in the film The Privileged Planet relating to geology, the atmosphere, the magnetic field, and other abiotic phenomena. We've seen that that life itself maintains the habitability of the earth in surprising ways. By means of coded instructions in their genomes, the tiniest of creatures play major roles in maintaining the essential cycles of the planet: the hydrologic cycle, nitrogen cycle, oxygen cycle, carbon cycle, and more.
Evolutionists may weave stories about how these remarkable interactions arose gradually as life emerged and progressed. The instances above, though, should call into question whether any life could have subsisted on a bare earth without at least some of these processes already in operation. When these observations are combined with the other evidences of fine-tuning in the earth, the laws of physics, and the universe, the inference to design seems irresistible.
Evolution News & Views February 14, 2016 12:03 AM
Last week we discussed how microbes maintain the viability of life on our planet ("How Microbes Make Earth Habitable"). In the same vein, more news just arrived about the carbon and nitrogen cycles.
Following up on MIT's findings about plankton taking carbon to the ocean bottom, Ohio State has just concluded from the three-year Tara Oceans oceanography expedition that plankton -- and some viruses -- are "key to carrying carbon" from the atmosphere down to the seafloor sediments. They took pictures of microbes at different depths to learn which ones are carrying carbon downward as they sink to the bottom. The research has helped scientists understand "the interplay of organisms in the ocean and of their role in the health of the planet."
As for nitrogen, Current Biology posted a Primer on "The Nitrogen Cycle," confirming that it "is entirely controlled by microbial activities." Before man started producing chemical fertilizers, "nearly all of the reactive nitrogen in the biosphere was generated and recycled by microorganisms."
Microbes Follow Icebergs
Another interesting interaction between geology and life was reported by the BBC News. Mark Kinver writes that "Giant icebergs play [a] 'major role' in [the] ocean carbon cycle." An aerial image shows a brilliant bloom of phytoplankton following one such giant iceberg in its wake. What's happening? The bloom is "triggered by the distribution of nutrients -- such as iron -- from an iceberg's meltwater." What this signifies is important:
"We estimate that giant icebergs account for between 10% and 20% of the actual vertical rate of carbon going from the surface to the deep (Southern) Ocean," he suggested....
Plankton scientist Dr Richard Kirby, who was not involved in this study, observed: "The phytoplankton at the sunlit surface of the sea has played a central role in the sequestration of carbon over millennia to affect the atmospheric concentration of this greenhouse gas, and so the Earth's climate.
"This interesting paper shows how much we still have to learn about these microscopic organisms, and how a changing climate may affect them, and also the food web they support." [Emphasis added.]
Bacteria Attack Lignin
Readers of Evolution News may remember Ann Gauger and Matt Leisola's design inference about lignin, the complex molecule that gives wood its strength. They argued that no organism has exploited this energy-rich substance -- which is good news for us, because "the indigestibility of lignin may be an essential requirement for the balance of life," Gauger wrote. "Lignin slows the degradation of wood, thus allowing the buildup of humus in the soil, which in turn permits plant growth and all resulting life that depends on plants."
Now, news from Rice University says that bacteria use a "tag team" approach to break apart this complex substance that locks up more than half a plant's sugar and holds a third of the carbon in biomass. This finding does not impact the conclusions of Gauger and Leisola, because the bacteria "chew through" the lignin to get to the cellulose they can digest. But "it's a very slow process, which is why it can take years for dead trees to decompose." The rate of decomposition of this energy-rich substance is what's interesting for considerations of planetary carbon cycling and habitability.
Bacteria Prepare the Land for Habitation
Another interesting interaction of microbes with geology happens on land. Biocrusts are accumulations of cryptic bacteria that inhabit the surfaces of arid soils. A paper in Nature Communications notes the ecological impact of these microbial habitats:
Much of the arid soil surfaces can be populated by cryptic photosynthetic assemblages known as biological soil crusts (or biocrusts), which are known to impart stability against erosion, to modify the hydrological properties of soils, and to contribute significantly to arid land fertility.
Researchers from Arizona and California found that the bacteria, mostly the nitrogen-fixing variety, produce a secondary metabolite called scytonemin that acts as a "sunscreen". It strongly absorbs solar radiation and dissipates it as heat, raising soil temperatures as much as 10°C, an effect that is "not without consequences" for soil microbial communities. While potentially making deserts more arid, this effect is good for temperate and arctic zones: "biocrusts in cold climates, that is, in polar settings or during winter months when activity is limited by temperature, the warming can be expected to be largely beneficial to biological entities."
About 41 percent of the earth's surface is arid, and this is where biocrusts figure prominently. By producing this sunscreen molecule, bacteria protect the soil from harmful radiation while simultaneously raising the temperature in cold arid lands to promote the growth of complex plants in ecological succession -- all this while stabilizing the soil, reducing erosion and fixing nitrogen that higher plants need. It's another case that has just come to light of global benefit from the world's smallest organisms.
For these reasons, microbial effects on land surface albedo may have global scale repercussions historically and in the present, and should be evaluated in models of planetary radiation budgets as a new twist of biosphere-climate feedback interactions. This may shed some light into the apparent inconsistency in temperature changes recorded in arid lands. Contrary to model predictions, temperature has been shown to increase when removing vegetation there, an apparent paradox that could potentially be explained by biocrust colonization. Based on estimates of the global biomass of cyanobacteria in soil biocrusts, one can easily calculate that there must currently exist about 15 million metric tons of scytonemin at work, warming soil surfaces worldwide.
Big Animals Help Earth's Habitability, Too
From orbit, a bear would appear as small as a microbe. Current Biology published another indication that all living things, even the big ones, have a stake in keeping the earth habitable. In "Megafauna move nutrients uphill," Michael Gross points to research about whales, salmon, birds and bears that reveal large animals' roles in moving phosphorus and nitrogenous compounds from the deep ocean to the mountains. These "ecosystem engineers" perform an "important ecosystem service" by distributing nutrients to higher elevations.
Given the laws of gravity and the hydrological cycle, there is a strong likelihood that nutrients available on land, even though they may go through many cycles around the food web, will eventually be washed out to the sea. In the oceans, there is the risk that they will drop out of the photic zone and reach the sea floor, where they will be buried in sediment that may only be returned to circulation on geological timescales, some tens or hundreds of millions of years later.
Animals can make important contributions to stem this flow, as was first reported for whales back in 2010 (Curr. Biol. (2010) 20, R541). Researchers studying the ecology of sperm whales found that they harvest nutrients such as iron from great depths (often more than 1,000 metres), where they hunt cephalopods, but release them when they defecate near the surface.
The nutrients are incorporated into microbes, plankton, and fish that become prey for birds and mammals. These larger animals, in turn, transport the nutrients up rivers and mountains. Although Michael Gross focuses on how humans are disrupting this natural system, one can only stand in awe of how the living web distributes the very atoms and molecules needed for complex life around the globe.
Tiny Creatures, Major Roles
It takes more than a rocky planet in a habitable zone to sustain life. Some twenty factors are listed in the film The Privileged Planet relating to geology, the atmosphere, the magnetic field, and other abiotic phenomena. We've seen that that life itself maintains the habitability of the earth in surprising ways. By means of coded instructions in their genomes, the tiniest of creatures play major roles in maintaining the essential cycles of the planet: the hydrologic cycle, nitrogen cycle, oxygen cycle, carbon cycle, and more.
Evolutionists may weave stories about how these remarkable interactions arose gradually as life emerged and progressed. The instances above, though, should call into question whether any life could have subsisted on a bare earth without at least some of these processes already in operation. When these observations are combined with the other evidences of fine-tuning in the earth, the laws of physics, and the universe, the inference to design seems irresistible.
Is it time to give Darwin the pink slip.
On Darwin Day, Darwinism Is Well Past Its "Sell By" Date:
Michael Denton February 12, 2016 2:04 AM
Today is Darwin Day, marking the birthday of Charles Darwin, who is celebrated around the world as a secular saint. Everywhere there will be eulogies to neo-Darwinism as a philosophy, touting the support it provides to the mechanistic worldview and the notion that life is an artifact of time and chance. Darwinism in that sense, almost akin to a faith, is indeed going strong.
Yet Darwinism as a scientific theory remains, as it always has been, a highly speculative evolutionary model. My new book, Evolution: Still a Theory in Crisis, makes that clear. I document in detail old ideas and new research that come together to severely undermine classic Darwinism and point to a new non-Darwinian paradigm for biology in the 21st century.
As the book shows, key features of the biological realm flatly contradict the Darwinian mechanism of natural selection and the notion that all features of living things are or were in some ancestral form adaptive. My new book is a sequel to my 1985 work, Evolution: A Theory in Crisis , and it shows how the crisis has deepened over the past three decades.To understand the core weakness of the Darwinian worldview, it is important to understand what Darwinian natural selection requires. The process will work its magic, building up functional structures in organisms, only when two very strict conditions are met: First, the structure must be adaptive -- that is, helpful to the organism in flourishing in its environment -- and second, there must be a continuum of structures, functional all along the way, leading from an ancestor species to the descendent.
That is, the thing we are trying to explain must in some way help the creature survive, and between the creature and the creature's ancestor there must be a gradual change, each step of which is stable and enhances fitness, or success in reproduction.
Problem number one is that there are a great number of complex structures in nature that are not led up to by known functional pathways, and imagining what these pathways might have been is in most cases very hard. But this challenge is greatly compounded by an additional problem: that in many cases complex structures convey not the slightest evidence that they ever performed an adaptive function in putative ancestral forms. This may come as a surprise to the student of evolution. The trade language of biology has focused on the concepts of adaptation, fitness, and utility for so long that it has in a sense blinded us to the universe of apparently non-adaptive order that permeates the entire organic realm.
For example, what is the adaptive fitness of the shape of a maple leaf? Or the shape of any leaf, for that matter? Nor are examples of seemingly non-adaptive order limited to the shapes of leaves. Some of the best examples are embedded deep within the biological world -- among the characteristics that define and separate the basic kinds or types of plants and animals from each other.
Consider the pentadactyl (five-finger) design of the tetrapod limb, witnessed in the human arm and leg: one bone (the humerus in the upper arm, the femur in the upper leg), two bones (the radius and ulna in your lower arm, the tibia and fibula in the lower leg ), five fingers and five toes. This unique design occurs in the fore and hind limbs of all tetrapod (four-limbed) vertebrates, including human beings.
It is clear that in all tetrapod limbs the same basic design has been adapted to very different uses. However, given that the adaptive forms of the fore and hind limbs differ to some degree in every known tetrapod, it is very difficult to explain how the underlying pattern could have been arrived at so as to serve some adaptive end in a hypothetical fore and hind limb of an ancestral tetrapod. The Darwinian explanation, attributing the underlying structure to previous rounds of natural selection, is self-evidently ad hoc.
If we can't explain what specific adaptive function the pentadactyl design serves in any known extant or extinct species of tetrapod, there are no grounds for the Darwinian claim that there was some hypothetical species in some hypothetical environment where this unique design did serve some mysteriously obscure adaptive function in both limbs. In this case, even "just so stories" can't legitimate the Darwinian account.
The challenge to the Darwinian framework is not restricted to the tetrapod limb, but applies almost universally to a veritable universe of other novel structures -- the insect body plan, the concentric whorl pattern underlying all flowers, and the enucleated red blood cell found in all mammals, which was the subject of my own doctoral work at King's College in London.
Contributing further to the challenge inherent in so much non-adaptive order are revelations from the new field of evolutionary developmental biology (evo-devo). We now know that the paths of evolution have been highly constrained by a set of universally conserved developmental genetic mechanisms that transcend any immediate adaptive utility. Moreover, evo-devo implies that in the case of many novelties, internal constraints have played a decisive role in evolutionary origins.
In my new book, I detail vast quantities of evidence from the most up-to-date scientific literature, all supporting the radical idea that Darwinism played a very minor role in the history of life, and that evolutionary biology in the 21st century will have to seek an entirely new causal framework.
Darwinists will of course continue to insist that classic Darwinism can provide a completely plausible explanation of all evolutionary phenomena. But the reality is that Darwin's theory is well past its "sell by" date. By Darwin Day next year, we can confidently predict the situation will appear no less dire, and likely even more so.
Editor's note: Get your copy of Evolution: Still a Theory in Crisis now. For a limited time, you'll enjoy a 30 percent discount at CreateSpace by using the discount code QBDHMYJH.
Michael Denton February 12, 2016 2:04 AM
Today is Darwin Day, marking the birthday of Charles Darwin, who is celebrated around the world as a secular saint. Everywhere there will be eulogies to neo-Darwinism as a philosophy, touting the support it provides to the mechanistic worldview and the notion that life is an artifact of time and chance. Darwinism in that sense, almost akin to a faith, is indeed going strong.
Yet Darwinism as a scientific theory remains, as it always has been, a highly speculative evolutionary model. My new book, Evolution: Still a Theory in Crisis, makes that clear. I document in detail old ideas and new research that come together to severely undermine classic Darwinism and point to a new non-Darwinian paradigm for biology in the 21st century.
As the book shows, key features of the biological realm flatly contradict the Darwinian mechanism of natural selection and the notion that all features of living things are or were in some ancestral form adaptive. My new book is a sequel to my 1985 work, Evolution: A Theory in Crisis , and it shows how the crisis has deepened over the past three decades.To understand the core weakness of the Darwinian worldview, it is important to understand what Darwinian natural selection requires. The process will work its magic, building up functional structures in organisms, only when two very strict conditions are met: First, the structure must be adaptive -- that is, helpful to the organism in flourishing in its environment -- and second, there must be a continuum of structures, functional all along the way, leading from an ancestor species to the descendent.
That is, the thing we are trying to explain must in some way help the creature survive, and between the creature and the creature's ancestor there must be a gradual change, each step of which is stable and enhances fitness, or success in reproduction.
Problem number one is that there are a great number of complex structures in nature that are not led up to by known functional pathways, and imagining what these pathways might have been is in most cases very hard. But this challenge is greatly compounded by an additional problem: that in many cases complex structures convey not the slightest evidence that they ever performed an adaptive function in putative ancestral forms. This may come as a surprise to the student of evolution. The trade language of biology has focused on the concepts of adaptation, fitness, and utility for so long that it has in a sense blinded us to the universe of apparently non-adaptive order that permeates the entire organic realm.
For example, what is the adaptive fitness of the shape of a maple leaf? Or the shape of any leaf, for that matter? Nor are examples of seemingly non-adaptive order limited to the shapes of leaves. Some of the best examples are embedded deep within the biological world -- among the characteristics that define and separate the basic kinds or types of plants and animals from each other.
Consider the pentadactyl (five-finger) design of the tetrapod limb, witnessed in the human arm and leg: one bone (the humerus in the upper arm, the femur in the upper leg), two bones (the radius and ulna in your lower arm, the tibia and fibula in the lower leg ), five fingers and five toes. This unique design occurs in the fore and hind limbs of all tetrapod (four-limbed) vertebrates, including human beings.
It is clear that in all tetrapod limbs the same basic design has been adapted to very different uses. However, given that the adaptive forms of the fore and hind limbs differ to some degree in every known tetrapod, it is very difficult to explain how the underlying pattern could have been arrived at so as to serve some adaptive end in a hypothetical fore and hind limb of an ancestral tetrapod. The Darwinian explanation, attributing the underlying structure to previous rounds of natural selection, is self-evidently ad hoc.
If we can't explain what specific adaptive function the pentadactyl design serves in any known extant or extinct species of tetrapod, there are no grounds for the Darwinian claim that there was some hypothetical species in some hypothetical environment where this unique design did serve some mysteriously obscure adaptive function in both limbs. In this case, even "just so stories" can't legitimate the Darwinian account.
The challenge to the Darwinian framework is not restricted to the tetrapod limb, but applies almost universally to a veritable universe of other novel structures -- the insect body plan, the concentric whorl pattern underlying all flowers, and the enucleated red blood cell found in all mammals, which was the subject of my own doctoral work at King's College in London.
Contributing further to the challenge inherent in so much non-adaptive order are revelations from the new field of evolutionary developmental biology (evo-devo). We now know that the paths of evolution have been highly constrained by a set of universally conserved developmental genetic mechanisms that transcend any immediate adaptive utility. Moreover, evo-devo implies that in the case of many novelties, internal constraints have played a decisive role in evolutionary origins.
In my new book, I detail vast quantities of evidence from the most up-to-date scientific literature, all supporting the radical idea that Darwinism played a very minor role in the history of life, and that evolutionary biology in the 21st century will have to seek an entirely new causal framework.
Darwinists will of course continue to insist that classic Darwinism can provide a completely plausible explanation of all evolutionary phenomena. But the reality is that Darwin's theory is well past its "sell by" date. By Darwin Day next year, we can confidently predict the situation will appear no less dire, and likely even more so.
Editor's note: Get your copy of Evolution: Still a Theory in Crisis now. For a limited time, you'll enjoy a 30 percent discount at CreateSpace by using the discount code QBDHMYJH.
Another failed Darwinian prediction VII
The pentadactyl pattern and common descent:
The pentadactyl structure—five digits (four fingers and a thumb for humans) at the end of the limb structure—is one of the most celebrated proof texts for evolution. The pentadactyl structure is found throughout the tetrapods and its uses include flying, grasping, climbing and crawling. Such diverse activities, evolutionists reason, should require diverse limbs. There seems to be no reason why all should need a five digit limb. Why not three digits for some, eight for others, 13 for some others, and so forth? And yet they all are endowed with five digits. As Darwin explained, “What can be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include similar bones, in the same relative positions?” (Darwin, 382)
Such a suboptimal design must be an artefact of common descent—a suboptimal design that was handed down from a common ancestor rather than specifically designed for each species. And the common descent pattern formed by this structure is often claimed as strong evidence for evolution. (Berra, 21; Campbell et. al., 509; Futuyma, 47; Johnson and Losos, 298; Johnson and Raven, 286; Mayr, 26) One text calls it a “classic example” of evolutionary evidence. (Ridley, 45)
But this prediction is now known to be false as the digit structure in the tetrapods does not conform to the common descent pattern. In fact, appendages have various digit structures and they are distributed across the species in various ways. This is found both in extant species and in the fossil record. As evolutionist Stephen Jay Gould explained, “The conclusion seems inescapable, and an old ‘certainty’ must be starkly reversed.” (Gould)
This means that evolutionists cannot model the observed structures and pattern of distribution merely as a consequence of common descent. Instead, a complicated evolutionary history is required (Brown) where the pentadactyl structure re-evolves in different lineages, and appendages evolve, are lost, and then evolve again. And as one recent study concluded, “Our phylogenetic results support independent instances of complete limb loss as well as multiple instances of digit and external ear opening loss and re-acquisition. Even more striking, we find strong statistical support for the re-acquisition of a pentadactyl body form from a digit-reduced ancestor. … The results of our study join a nascent body of literature showing strong statistical support for character loss, followed by evolutionary re-acquisition of complex structures associated with a generalized pentadactyl body form.” (Siler and Brown)
References
Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.
Brown, R., et. al. 2012. “Species delimitation and digit number in a North African skink.” Ecology and Evolution 2:2962-73.
Campbell, Neil, et. al. 2011. Biology. 5th ed. San Francisco: Pearson.
Darwin, Charles. 1872. The Origin of Species. 6th ed. London: John Murray.
http://darwin-online.org.uk/content/frameset?itemID=F391&viewtype=text&pageseq=1
Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.
Gould, Steven Jay. 1991. “Eight (or Fewer) Little Piggies.” Natural History 100:22-29.
Johnson, G., J. Losos. 2008. The Living World. 5th ed. New York: McGraw-Hill.
Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.
Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.
Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.
Siler C., R. Brown. 2011. “Evidence for repeated acquisition and loss of complex body-form characters in an insular clade of Southeast Asian semi-fossorial skinks.” Evolution 65:2641-2663.
The pentadactyl structure—five digits (four fingers and a thumb for humans) at the end of the limb structure—is one of the most celebrated proof texts for evolution. The pentadactyl structure is found throughout the tetrapods and its uses include flying, grasping, climbing and crawling. Such diverse activities, evolutionists reason, should require diverse limbs. There seems to be no reason why all should need a five digit limb. Why not three digits for some, eight for others, 13 for some others, and so forth? And yet they all are endowed with five digits. As Darwin explained, “What can be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include similar bones, in the same relative positions?” (Darwin, 382)
Such a suboptimal design must be an artefact of common descent—a suboptimal design that was handed down from a common ancestor rather than specifically designed for each species. And the common descent pattern formed by this structure is often claimed as strong evidence for evolution. (Berra, 21; Campbell et. al., 509; Futuyma, 47; Johnson and Losos, 298; Johnson and Raven, 286; Mayr, 26) One text calls it a “classic example” of evolutionary evidence. (Ridley, 45)
But this prediction is now known to be false as the digit structure in the tetrapods does not conform to the common descent pattern. In fact, appendages have various digit structures and they are distributed across the species in various ways. This is found both in extant species and in the fossil record. As evolutionist Stephen Jay Gould explained, “The conclusion seems inescapable, and an old ‘certainty’ must be starkly reversed.” (Gould)
This means that evolutionists cannot model the observed structures and pattern of distribution merely as a consequence of common descent. Instead, a complicated evolutionary history is required (Brown) where the pentadactyl structure re-evolves in different lineages, and appendages evolve, are lost, and then evolve again. And as one recent study concluded, “Our phylogenetic results support independent instances of complete limb loss as well as multiple instances of digit and external ear opening loss and re-acquisition. Even more striking, we find strong statistical support for the re-acquisition of a pentadactyl body form from a digit-reduced ancestor. … The results of our study join a nascent body of literature showing strong statistical support for character loss, followed by evolutionary re-acquisition of complex structures associated with a generalized pentadactyl body form.” (Siler and Brown)
References
Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.
Brown, R., et. al. 2012. “Species delimitation and digit number in a North African skink.” Ecology and Evolution 2:2962-73.
Campbell, Neil, et. al. 2011. Biology. 5th ed. San Francisco: Pearson.
Darwin, Charles. 1872. The Origin of Species. 6th ed. London: John Murray.
http://darwin-online.org.uk/content/frameset?itemID=F391&viewtype=text&pageseq=1
Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.
Gould, Steven Jay. 1991. “Eight (or Fewer) Little Piggies.” Natural History 100:22-29.
Johnson, G., J. Losos. 2008. The Living World. 5th ed. New York: McGraw-Hill.
Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.
Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.
Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.
Siler C., R. Brown. 2011. “Evidence for repeated acquisition and loss of complex body-form characters in an insular clade of Southeast Asian semi-fossorial skinks.” Evolution 65:2641-2663.
Friday 12 February 2016
Thursday 11 February 2016
Choosing education over indoctrination.
NCSE's Disinformation Campaign Aside, Mississippi Bill Is an Opportunity for Educational Excellence
Sarah Chaffee February 11, 2016 11:05 AM
After the filing of an academic freedom bill in Mississippi, HB 50, the Jackson Clarion-Ledger published a piece featuring some common misconceptions. And predictably, the National Center for Science Education (NCSE), the nation's top Darwin lobby group, claimed the bill is "anti-science." Permit me to alleviate concerns and clarify the nature of the legislation.
It's always helpful to read what a bill actually says. This one states, "[T]eachers shall be permitted to help students understand, analyze, critique and review in an objective manner the scientific strengths and scientific weaknesses of existing scientific theories covered in the course being taught..."
So, first of all, the bill only authorizes teachers to present scientific information regarding controversial theories. Areas outside of scientific strengths and weaknesses are outside of the legislation, which consequently would not protect instructors who teach about such matters.
Yet the NCSE claims:
House Bill 50, introduced in the Mississippi House of Representatives and referred to the House Education Committee on February 8, 2016, would, if enacted, allow science teachers with idiosyncratic opinions to teach anything they pleased -- and prohibit responsible educational authorities from intervening.
That is flatly false. NCSE Deputy Director Glenn Branch echoed the fiction, telling the Clarion Ledger, "There's no reason a teacher couldn't say that women or blacks are inferior, or ... that the Earth was flat or the sun goes around the Earth, and then couldn't be shut down by the administration."
What? Is Branch saying he thinks that, in 2016, racism, sexism, and geocentrism count as "scientific" ideas? Because that's the only way they could conceivably be protected under the language of the bill. Last time I checked, there were no scientific articles being published in mainstream peer-reviewed journals critical of "round-earth theory" -- but there is indeed mainstream criticism of classic Darwinian theory.
For information on the scientific weaknesses in modern evolutionary science, see Casey Luskin's accounts of uncertainty in origins science and controversy over evolution. And check out the Scientific Dissent from Darwinism list (with more than 900 PhD signers).
There also seems to be some confusion about whether the bill would allow teachers to discuss creationism or religious beliefs. The answer is no. Public schools cannot legally teach creationism. The Supreme Court has long held that it is unconstitutional to teach religion in the classroom and that creationism is a religious belief (Edwards v. Aguillard). Remember, the bill only authorizes "the teaching of scientific information and shall not be construed to promote any religious or nonreligious doctrine."
I don't see how that could be clearer. Promoting a religious idea such as creationism is not protected under this law. As Casey Luskin has pointed out: "If you're teaching religion, then you're not protected by an academic freedom bill. Since creationism has been ruled a religious belief by the Supreme Court, teachers who teach it would not be protected."
Neither does the bill authorize teachers to introduce intelligent design. First of all, teaching the strengths and weaknesses of neo-Darwinian evolutionary theory is not the same as teaching about ID. Perhaps more importantly, the bill only permits the teaching of scientific strengths and weaknesses of theories that are "covered in the course being taught within the curriculum framework developed by the State Board of Education." Since intelligent design is not part of the curriculum anywhere in Mississippi, it would not be protected by the bill (indeed, we oppose pushing intelligent design into public school classrooms).
It's shame that a group like the NCSE enjoys such success in spreading misinformation. Mississippi's legislation would advance quality science education in the state. In a joint issue on the theme of reform in STEM (Science, Technology, Engineering, Math) education, Nature and Scientific American noted, "[S]tudents gain a much deeper understanding of science when they actively grapple with questions than when they passively listen to answers."
Make no mistake, Mississippi's HB 50 is not "anti-science" as the NCSE claims. This academic freedom legislation would do a service to educational excellence in science. It does a disservice to students, and to the facts, to say otherwise.
Sarah Chaffee February 11, 2016 11:05 AM
After the filing of an academic freedom bill in Mississippi, HB 50, the Jackson Clarion-Ledger published a piece featuring some common misconceptions. And predictably, the National Center for Science Education (NCSE), the nation's top Darwin lobby group, claimed the bill is "anti-science." Permit me to alleviate concerns and clarify the nature of the legislation.
It's always helpful to read what a bill actually says. This one states, "[T]eachers shall be permitted to help students understand, analyze, critique and review in an objective manner the scientific strengths and scientific weaknesses of existing scientific theories covered in the course being taught..."
So, first of all, the bill only authorizes teachers to present scientific information regarding controversial theories. Areas outside of scientific strengths and weaknesses are outside of the legislation, which consequently would not protect instructors who teach about such matters.
Yet the NCSE claims:
House Bill 50, introduced in the Mississippi House of Representatives and referred to the House Education Committee on February 8, 2016, would, if enacted, allow science teachers with idiosyncratic opinions to teach anything they pleased -- and prohibit responsible educational authorities from intervening.
That is flatly false. NCSE Deputy Director Glenn Branch echoed the fiction, telling the Clarion Ledger, "There's no reason a teacher couldn't say that women or blacks are inferior, or ... that the Earth was flat or the sun goes around the Earth, and then couldn't be shut down by the administration."
What? Is Branch saying he thinks that, in 2016, racism, sexism, and geocentrism count as "scientific" ideas? Because that's the only way they could conceivably be protected under the language of the bill. Last time I checked, there were no scientific articles being published in mainstream peer-reviewed journals critical of "round-earth theory" -- but there is indeed mainstream criticism of classic Darwinian theory.
For information on the scientific weaknesses in modern evolutionary science, see Casey Luskin's accounts of uncertainty in origins science and controversy over evolution. And check out the Scientific Dissent from Darwinism list (with more than 900 PhD signers).
There also seems to be some confusion about whether the bill would allow teachers to discuss creationism or religious beliefs. The answer is no. Public schools cannot legally teach creationism. The Supreme Court has long held that it is unconstitutional to teach religion in the classroom and that creationism is a religious belief (Edwards v. Aguillard). Remember, the bill only authorizes "the teaching of scientific information and shall not be construed to promote any religious or nonreligious doctrine."
I don't see how that could be clearer. Promoting a religious idea such as creationism is not protected under this law. As Casey Luskin has pointed out: "If you're teaching religion, then you're not protected by an academic freedom bill. Since creationism has been ruled a religious belief by the Supreme Court, teachers who teach it would not be protected."
Neither does the bill authorize teachers to introduce intelligent design. First of all, teaching the strengths and weaknesses of neo-Darwinian evolutionary theory is not the same as teaching about ID. Perhaps more importantly, the bill only permits the teaching of scientific strengths and weaknesses of theories that are "covered in the course being taught within the curriculum framework developed by the State Board of Education." Since intelligent design is not part of the curriculum anywhere in Mississippi, it would not be protected by the bill (indeed, we oppose pushing intelligent design into public school classrooms).
It's shame that a group like the NCSE enjoys such success in spreading misinformation. Mississippi's legislation would advance quality science education in the state. In a joint issue on the theme of reform in STEM (Science, Technology, Engineering, Math) education, Nature and Scientific American noted, "[S]tudents gain a much deeper understanding of science when they actively grapple with questions than when they passively listen to answers."
Make no mistake, Mississippi's HB 50 is not "anti-science" as the NCSE claims. This academic freedom legislation would do a service to educational excellence in science. It does a disservice to students, and to the facts, to say otherwise.
Darwinism takes it on the chin yet again.
On the Origin of Chins
Ann Gauger February 11, 2016 3:48 AM
ere's an evolutionary puzzle I had never thought about. Why do we have chins?
That bony protuberance at the end of your jaw may be hidden by a beard or a fleshy throat, but it is still there. Chimpanzees don't have chins, neither do gorillas, orangutans, spider monkeys, dogs, horses, frogs, or fish. Did you know that only humans have chins? I didn't, but then I never studied vertebrate anatomy. It seems that having a chin is diagnostic of being a modern human. Even Neanderthals may have lacked chins, though this is a matter of dispute.
So the question of the origin of chins quite naturally arises. It turns out that a number of scientists have thought about it. Writing in the journal Evolutionary Anthropology, James Pampush and David Daegling discuss all the ways researchers have tried to come up with an explanation for why we have chins. The article is tellingly titled, "The Enduring Puzzle of the Human Chin."
The story has caught the attention of science journalists. The funniest is Ed Yong over at The Atlantic. Unfortunately he has taken all the chin jokes that I can think of. Melissa Hogenboom also wrote a piece for BBC Earth.
All those scientists cannot find a good evolutionary answer to the question. A chin doesn't make our jaws stronger for chewing. Or for taking punches -- that's another theory. It doesn't aid with speech. It isn't involved with sexual selection since both males and females have chins (thank goodness). It doesn't open up our airways.
It isn't the result of living in groups and needing to reduce testosterone. That's right -- the hypothesis is that less testosterone allows us to live in social groups. It's called self-domestication. Reduced testosterone pulls back the mid face and exposes the chin, so the theory goes. Except that men have higher levels of testosterone than females and have larger chins, not smaller ones.
The last hypothesis: having a chin is a spandrel -- a side effect of another adaptive change. The idea is that when we started eating soft food our jaws became weaker. The top part -- the maxilla -- shrank, and the teeth moved accordingly, but the mandible didn't shrink proportionately, and voilá, we have a chin! The trouble with this story is just that. It's a story, with no way of testing it. Well, there were some animal experiments, unpleasant ones, but those yielded no conclusive evidence.
The authors conclude:
Each of the proposals we have discussed falter either empirically or theoretically; some fail, to a degree, on both accounts... This should serve as motivation, not discouragement, for researchers to continue investigating this modern human peculiarity... perhaps understanding the chin will reveal some unexpected insight into what it means to be human.
Perhaps it does reveal something important about being human. Perhaps no adaptive explanation for chins exists, because they aren't adaptations -- they arise from aesthetic considerations. Without a chin there would be no delicate curve of the neck in Swan Lake, no graceful oval shape to the face, no balance or proportion in portraits. It's not just that we are used to chins. We respond to proportion in all things, be it architecture, landscapes, or the spiral petals of a rose. The chin balances the face.
Now I've gone all serious when all I intended was light-hearted comments on looking for adaptations in all the wrong places. Chin up. I'm done.
Ann Gauger February 11, 2016 3:48 AM
ere's an evolutionary puzzle I had never thought about. Why do we have chins?
That bony protuberance at the end of your jaw may be hidden by a beard or a fleshy throat, but it is still there. Chimpanzees don't have chins, neither do gorillas, orangutans, spider monkeys, dogs, horses, frogs, or fish. Did you know that only humans have chins? I didn't, but then I never studied vertebrate anatomy. It seems that having a chin is diagnostic of being a modern human. Even Neanderthals may have lacked chins, though this is a matter of dispute.
So the question of the origin of chins quite naturally arises. It turns out that a number of scientists have thought about it. Writing in the journal Evolutionary Anthropology, James Pampush and David Daegling discuss all the ways researchers have tried to come up with an explanation for why we have chins. The article is tellingly titled, "The Enduring Puzzle of the Human Chin."
The story has caught the attention of science journalists. The funniest is Ed Yong over at The Atlantic. Unfortunately he has taken all the chin jokes that I can think of. Melissa Hogenboom also wrote a piece for BBC Earth.
All those scientists cannot find a good evolutionary answer to the question. A chin doesn't make our jaws stronger for chewing. Or for taking punches -- that's another theory. It doesn't aid with speech. It isn't involved with sexual selection since both males and females have chins (thank goodness). It doesn't open up our airways.
It isn't the result of living in groups and needing to reduce testosterone. That's right -- the hypothesis is that less testosterone allows us to live in social groups. It's called self-domestication. Reduced testosterone pulls back the mid face and exposes the chin, so the theory goes. Except that men have higher levels of testosterone than females and have larger chins, not smaller ones.
The last hypothesis: having a chin is a spandrel -- a side effect of another adaptive change. The idea is that when we started eating soft food our jaws became weaker. The top part -- the maxilla -- shrank, and the teeth moved accordingly, but the mandible didn't shrink proportionately, and voilá, we have a chin! The trouble with this story is just that. It's a story, with no way of testing it. Well, there were some animal experiments, unpleasant ones, but those yielded no conclusive evidence.
The authors conclude:
Each of the proposals we have discussed falter either empirically or theoretically; some fail, to a degree, on both accounts... This should serve as motivation, not discouragement, for researchers to continue investigating this modern human peculiarity... perhaps understanding the chin will reveal some unexpected insight into what it means to be human.
Perhaps it does reveal something important about being human. Perhaps no adaptive explanation for chins exists, because they aren't adaptations -- they arise from aesthetic considerations. Without a chin there would be no delicate curve of the neck in Swan Lake, no graceful oval shape to the face, no balance or proportion in portraits. It's not just that we are used to chins. We respond to proportion in all things, be it architecture, landscapes, or the spiral petals of a rose. The chin balances the face.
Now I've gone all serious when all I intended was light-hearted comments on looking for adaptations in all the wrong places. Chin up. I'm done.
Wednesday 10 February 2016
On Darwinists' The emperor's new robes defense.
Darwinian Debating Device #18: The “You’re Too Stupid to Understand Why I’m Smarter than You” Dismissal:
May 10, 2015 Posted by Barry Arrington under Darwinian Debating Devices
DDD # 18 is a particularly contemptible from of ad hominem, which Mark Frank and Elizabeth Liddle do us the service of demonstrating in the combox to this post. In the post Dr. Torley refers to Darwin’s Doubt by Dr. Stephen C. Meyer, which explains many of the shortcomings of various Darwinian narratives. Frank and Liddle tag team for a DDD #18:
Mark Frank:
[Meyer] explains perceived weaknesses in his understanding of evolutionary theory but gives no reason why design is a better alternative.
Liddle:
Exactly. His understanding of evolutionary theory is weak, and actual evolutionary theory is a better alternative.
Follow this link and take a look at what scientists who actually know what they are talking about have said about Darwin’s Doubt. A sample:
Darwin’s Doubt is by far the most up-to-date, accurate, and comprehensive review of the evidence from all relevant scientific fields that I have encountered in more than forty years of studying the Cambrian explosion. An engaging investigation of the origin of animal life and a compelling case for intelligent design.
Dr. Wolf-Ekkehard Lönnig, Senior Scientist Emeritus (Biologist) at the Max Planck Institute for Plant Breeding Research
Darwin’s Doubt is an intriguing exploration of one of the most remarkable periods in the evolutionary history of life—the rapid efflorescence of complex body plans written in the fossils of the Burgess Shale . . . No matter what convictions one holds about evolution, Darwinism, or intelligent design, Darwin’s Doubt is a book that should be read, engaged, and discussed.
Dr. Scott Turner, Professor of Biology, State University of New York
Does anyone believe that numerous highly-credentialed scientists, many of whom specialize in biology, would recommend Meyer’s book if his “understanding of evolutionary theory is weak”? Of course not. What does this mean? It means that Elizabeth Liddle’s statement is false. I will leave it to others to debate whether she is merely too muddle-headed to understand that she has made an egregiously false ad hominem attack as a substitute for argument, or she knows the truth and has deliberately misled. The point is that either way, Liddle has avoided having to actually defend against Meyer’s claims by simply dismissing him as too stupid to understand why Darwinists like her are smarter than he. And that is contemptible.
May 10, 2015 Posted by Barry Arrington under Darwinian Debating Devices
DDD # 18 is a particularly contemptible from of ad hominem, which Mark Frank and Elizabeth Liddle do us the service of demonstrating in the combox to this post. In the post Dr. Torley refers to Darwin’s Doubt by Dr. Stephen C. Meyer, which explains many of the shortcomings of various Darwinian narratives. Frank and Liddle tag team for a DDD #18:
Mark Frank:
[Meyer] explains perceived weaknesses in his understanding of evolutionary theory but gives no reason why design is a better alternative.
Liddle:
Exactly. His understanding of evolutionary theory is weak, and actual evolutionary theory is a better alternative.
Follow this link and take a look at what scientists who actually know what they are talking about have said about Darwin’s Doubt. A sample:
Darwin’s Doubt is by far the most up-to-date, accurate, and comprehensive review of the evidence from all relevant scientific fields that I have encountered in more than forty years of studying the Cambrian explosion. An engaging investigation of the origin of animal life and a compelling case for intelligent design.
Dr. Wolf-Ekkehard Lönnig, Senior Scientist Emeritus (Biologist) at the Max Planck Institute for Plant Breeding Research
Darwin’s Doubt is an intriguing exploration of one of the most remarkable periods in the evolutionary history of life—the rapid efflorescence of complex body plans written in the fossils of the Burgess Shale . . . No matter what convictions one holds about evolution, Darwinism, or intelligent design, Darwin’s Doubt is a book that should be read, engaged, and discussed.
Dr. Scott Turner, Professor of Biology, State University of New York
Does anyone believe that numerous highly-credentialed scientists, many of whom specialize in biology, would recommend Meyer’s book if his “understanding of evolutionary theory is weak”? Of course not. What does this mean? It means that Elizabeth Liddle’s statement is false. I will leave it to others to debate whether she is merely too muddle-headed to understand that she has made an egregiously false ad hominem attack as a substitute for argument, or she knows the truth and has deliberately misled. The point is that either way, Liddle has avoided having to actually defend against Meyer’s claims by simply dismissing him as too stupid to understand why Darwinists like her are smarter than he. And that is contemptible.
Tuesday 9 February 2016
Darwinism's inquisitors on the march again
From Patrick Anderson at the Argus Leader, More Misinformation on Academic Freedom in South Dakota:
Sarah Chaffee February 9, 2016 1:03 PM
We've met reporter Patrick Anderson before. On the subject of academic freedom, his work has left much to be desired. Now Mr. Anderson is back, spreading more misinformation.
In January, Senator Jeff Monroe introduced Senate Bill 83, which noted:
No teacher may be prohibited from helping students understand, analyze, critique, or review in an objective scientific manner the strengths and weaknesses of scientific information presented in courses being taught which are aligned with the content standards established pursuant to § 13-3-48.
Unfortunately, the bill died in committee on Thursday. However, I would like to correct Anderson's inaccurate reporting about the bill in particular and the issue of academic freedom in science education generally.
First, academic freedom bills, such as SB 83, do not authorize the teaching of intelligent design.
On January 31, Anderson wrote for the Argus Leader:
The bill is an effort to protect educators who offer a different school of thought on some of the subjects outlined in the state's science standards, Monroe said.
But science teachers don't need the protection as long as they're working with theories based on factual evidence, said Julie Olson, a science teacher in Mitchell. Olson is president of the South Dakota Science Teachers Association.
"Science has got to be fact-based, it has to be evidence-based," Olson said. "Intelligent design isn't evidence-based, so it isn't science."
...
Olson wishes Monroe and other lawmakers behind the senate bill would be more direct about their intentions.
"I just hate the fact that they're trying to sneak in the discussion on intelligent design," Olson said. "If that's what they want taught they should at least say it."
Anderson allows this to go unchallenged. But no, the bill only would have permitted the teaching of scientific strengths and weaknesses on "scientific information presented in courses being taught which are aligned with the content standards established..." Since intelligent design is not part of the curriculum anywhere in South Dakota, it would not have been protected by the bill.
Teaching the strengths and weaknesses of neo-Darwinian evolutionary theory is not the same as teaching about ID. For instance, in discussing evolution, a teacher might talk about whether or not Galápagos finches provide evidence of macroevolution. But such a discussion would not present positive evidence for design. To demonstrate the validity of intelligent design, one must make a positive case for the theory.
Second, Discovery Institute does not support pushing intelligent design into public schools. In fact, we oppose it.
Patrick Anderson has misstated Discovery Institute's position before, claiming that Discovery Institute advocates teaching intelligent design in public schools on the evidence of our textbook, Discovering Intelligent Design, produced explicitly and exclusively for home and private schools.
This year, he's at it again, writing: "The bill [SB 83] is based on model legislation from the Discovery Institute, a group with a curriculum for teaching intelligent design." No, here is what the Introduction to the curriculum says:
A NOTE ON USE IN PUBLIC SCHOOLS
This supplemental textbook is not intended for use in public schools. ID is a scientific theory and is not religiously based, but we live in a highly charged political climate that is often hostile to ID. While ID should be perfectly legal to discuss in public schools, there are strong reasons not to push ID into the public school curriculum.
In particular, the priority of the ID movement is to see the theory progress and mature as a science. However, when the subject is forced into public schools, it tends to generate controversy, changing the topic from a scientific investigation into an emotional, politicized debate. This can result in persecution of ID proponents in the academy, ultimately preventing ID from gaining a fair hearing within the scientific community.
The Introduction goes on to quote our official policy on teaching ID in public schools, which we have stated again and again. We oppose mandating the teaching of intelligent design in public school science classroom, and have made that clear in our ID curriculum for home and private schools. Can this be any clearer?
Third, academic freedom legislation, such as Monroe's bill, doesn't authorize the teaching of creationism.
Anderson reports:
The proposal could make it easier for teachers to bring Creationism into a public school classroom, despite parts of the bill that disavow any association with religion, said Glenn Branch, deputy director of the National Center for Science Education....
"It's kind of a recipe to encourage teachers to go rogue," Branch said. "I admit that it's fairly unlikely that teachers are going to be doing that, but teachers are people too, and people have funny ideas."
...
... [T]he bill states it "may not be construed to promote any religious or nonreligious doctrine."
Authors give no direction for determining what the promotion of religious doctrine might look like, Branch said.
"It's like wearing big sign saying, 'ignore me,'" Branch said.
Again, no. The bill would not have authorized the teaching of creationism or other religious beliefs. The text notes it only would have protected "the teaching of scientific information and may not be construed to promote any religious or nonreligious doctrine, nor may these provisions be construed to promote discrimination against any religion, religious belief, nonreligion, or nonbelief."
Furthermore, the bill didn't need to give "direction for determining" what promotes religion because courts have already defined what constitutes promotion of religion. Branch is neither a lawyer nor a legislator. There is a long line of court cases that make clear what is permissible and what is not.
As Casey Luskin has pointed out, "[I]f you're teaching religion, then you're not protected by an academic freedom bill. Since creationism has been ruled a religious belief by the Supreme Court, teachers who teach it would not be protected." Clearly, South Dakota's legislation would not have authorized teaching creationism.
Finally, opponents hold that the academic freedom bill somehow would have subverted the state's science standards. Andersonreports, "Even without the religious implications of the bill, Monroe's proposal undermines the democratic process of approving curriculum standards for K-12 schools, [Glenn] Branch [deputy director of the National Center for Science Education] said."
The National Center for Science Education reports on their website:
Testifying against the bill was Wade Pogany, the executive director of the Associated School Boards of South Dakota, who told the committee, in the words of KELO AM radio (February 4, 2016), that "state and federal courts have ruled that teachers can't abandon the curriculum for their own beliefs."
But Branch's and Pogany's concerns have little relevance to SB 83.
First, such legislation does not "undermine the democratic process." The Board of Education in South Dakota isn't elected in the first place, but appointed and then confirmed by the Senate. It would seem just as democratic to have permissive legislation for academic freedom in science education passed through the legislature.
Additionally, the general public overwhelmingly supports teaching the scientific strengths and weaknesses of scientific theories in at least one area (Darwinian evolution) as evidenced by a recent SurveyMonkey nationwide poll. Eighty-one percent of respondents agreed that, "when teaching Darwin's theory of evolution, biology teachers should cover both scientific evidence that supports the theory and scientific evidence critical of the theory." Of those from the West North Central region (which includes South Dakota), 83 percent agreed.
Furthermore, this legislation was limited to "the strengths and weaknesses of scientific information presented in courses being taught which are aligned with the content standards established pursuant to § 13-3-48." This bill only applies to content that has already been approved by the Board of Education of South Dakota. It does not authorize the teaching of information on topics outside of the standards.
The Introduction to the South Dakota Science Standards notes:
The concepts and content in the science standards represent the most current research in science and science education. All theories are presented in a way that allow teachers to structure an experience around multiple pieces of scientific evidence and competing ideas to allow students to engage in an objective discussion. The theories are presented because they have a large body of scientific evidence that supports them. These 6 standards were developed in such a manner to encourage students to analyze all forms of scientific evidence and draw their own conclusions.
Academic freedom legislation is in agreement with the spirit and purposes of South Dakota's science standards.
So what would academic freedom legislation actually accomplish? As I have written here previously, it would permit teachers to foster an environment of scientific inquiry by educating students about the evidence on both sides of scientific issues. Where this approach to learning has been adopted already, it trains students to think analytically. It awakens interest in science by inviting students to confront relevant research themselves. And students who succeed in science courses in grades K-12 are surely more likely to pursue degrees in those fields.
Inquiry in the classroom paves the way for inquiry in the lab. Contrary to what Mr. Anderson has been telling readers of the Argus Leader, enacting academic freedom legislation would have done a service to educational excellence in South Dakota.
Sarah Chaffee February 9, 2016 1:03 PM
We've met reporter Patrick Anderson before. On the subject of academic freedom, his work has left much to be desired. Now Mr. Anderson is back, spreading more misinformation.
In January, Senator Jeff Monroe introduced Senate Bill 83, which noted:
No teacher may be prohibited from helping students understand, analyze, critique, or review in an objective scientific manner the strengths and weaknesses of scientific information presented in courses being taught which are aligned with the content standards established pursuant to § 13-3-48.
Unfortunately, the bill died in committee on Thursday. However, I would like to correct Anderson's inaccurate reporting about the bill in particular and the issue of academic freedom in science education generally.
First, academic freedom bills, such as SB 83, do not authorize the teaching of intelligent design.
On January 31, Anderson wrote for the Argus Leader:
The bill is an effort to protect educators who offer a different school of thought on some of the subjects outlined in the state's science standards, Monroe said.
But science teachers don't need the protection as long as they're working with theories based on factual evidence, said Julie Olson, a science teacher in Mitchell. Olson is president of the South Dakota Science Teachers Association.
"Science has got to be fact-based, it has to be evidence-based," Olson said. "Intelligent design isn't evidence-based, so it isn't science."
...
Olson wishes Monroe and other lawmakers behind the senate bill would be more direct about their intentions.
"I just hate the fact that they're trying to sneak in the discussion on intelligent design," Olson said. "If that's what they want taught they should at least say it."
Anderson allows this to go unchallenged. But no, the bill only would have permitted the teaching of scientific strengths and weaknesses on "scientific information presented in courses being taught which are aligned with the content standards established..." Since intelligent design is not part of the curriculum anywhere in South Dakota, it would not have been protected by the bill.
Teaching the strengths and weaknesses of neo-Darwinian evolutionary theory is not the same as teaching about ID. For instance, in discussing evolution, a teacher might talk about whether or not Galápagos finches provide evidence of macroevolution. But such a discussion would not present positive evidence for design. To demonstrate the validity of intelligent design, one must make a positive case for the theory.
Second, Discovery Institute does not support pushing intelligent design into public schools. In fact, we oppose it.
Patrick Anderson has misstated Discovery Institute's position before, claiming that Discovery Institute advocates teaching intelligent design in public schools on the evidence of our textbook, Discovering Intelligent Design, produced explicitly and exclusively for home and private schools.
This year, he's at it again, writing: "The bill [SB 83] is based on model legislation from the Discovery Institute, a group with a curriculum for teaching intelligent design." No, here is what the Introduction to the curriculum says:
A NOTE ON USE IN PUBLIC SCHOOLS
This supplemental textbook is not intended for use in public schools. ID is a scientific theory and is not religiously based, but we live in a highly charged political climate that is often hostile to ID. While ID should be perfectly legal to discuss in public schools, there are strong reasons not to push ID into the public school curriculum.
In particular, the priority of the ID movement is to see the theory progress and mature as a science. However, when the subject is forced into public schools, it tends to generate controversy, changing the topic from a scientific investigation into an emotional, politicized debate. This can result in persecution of ID proponents in the academy, ultimately preventing ID from gaining a fair hearing within the scientific community.
The Introduction goes on to quote our official policy on teaching ID in public schools, which we have stated again and again. We oppose mandating the teaching of intelligent design in public school science classroom, and have made that clear in our ID curriculum for home and private schools. Can this be any clearer?
Third, academic freedom legislation, such as Monroe's bill, doesn't authorize the teaching of creationism.
Anderson reports:
The proposal could make it easier for teachers to bring Creationism into a public school classroom, despite parts of the bill that disavow any association with religion, said Glenn Branch, deputy director of the National Center for Science Education....
"It's kind of a recipe to encourage teachers to go rogue," Branch said. "I admit that it's fairly unlikely that teachers are going to be doing that, but teachers are people too, and people have funny ideas."
...
... [T]he bill states it "may not be construed to promote any religious or nonreligious doctrine."
Authors give no direction for determining what the promotion of religious doctrine might look like, Branch said.
"It's like wearing big sign saying, 'ignore me,'" Branch said.
Again, no. The bill would not have authorized the teaching of creationism or other religious beliefs. The text notes it only would have protected "the teaching of scientific information and may not be construed to promote any religious or nonreligious doctrine, nor may these provisions be construed to promote discrimination against any religion, religious belief, nonreligion, or nonbelief."
Furthermore, the bill didn't need to give "direction for determining" what promotes religion because courts have already defined what constitutes promotion of religion. Branch is neither a lawyer nor a legislator. There is a long line of court cases that make clear what is permissible and what is not.
As Casey Luskin has pointed out, "[I]f you're teaching religion, then you're not protected by an academic freedom bill. Since creationism has been ruled a religious belief by the Supreme Court, teachers who teach it would not be protected." Clearly, South Dakota's legislation would not have authorized teaching creationism.
Finally, opponents hold that the academic freedom bill somehow would have subverted the state's science standards. Andersonreports, "Even without the religious implications of the bill, Monroe's proposal undermines the democratic process of approving curriculum standards for K-12 schools, [Glenn] Branch [deputy director of the National Center for Science Education] said."
The National Center for Science Education reports on their website:
Testifying against the bill was Wade Pogany, the executive director of the Associated School Boards of South Dakota, who told the committee, in the words of KELO AM radio (February 4, 2016), that "state and federal courts have ruled that teachers can't abandon the curriculum for their own beliefs."
But Branch's and Pogany's concerns have little relevance to SB 83.
First, such legislation does not "undermine the democratic process." The Board of Education in South Dakota isn't elected in the first place, but appointed and then confirmed by the Senate. It would seem just as democratic to have permissive legislation for academic freedom in science education passed through the legislature.
Additionally, the general public overwhelmingly supports teaching the scientific strengths and weaknesses of scientific theories in at least one area (Darwinian evolution) as evidenced by a recent SurveyMonkey nationwide poll. Eighty-one percent of respondents agreed that, "when teaching Darwin's theory of evolution, biology teachers should cover both scientific evidence that supports the theory and scientific evidence critical of the theory." Of those from the West North Central region (which includes South Dakota), 83 percent agreed.
Furthermore, this legislation was limited to "the strengths and weaknesses of scientific information presented in courses being taught which are aligned with the content standards established pursuant to § 13-3-48." This bill only applies to content that has already been approved by the Board of Education of South Dakota. It does not authorize the teaching of information on topics outside of the standards.
The Introduction to the South Dakota Science Standards notes:
The concepts and content in the science standards represent the most current research in science and science education. All theories are presented in a way that allow teachers to structure an experience around multiple pieces of scientific evidence and competing ideas to allow students to engage in an objective discussion. The theories are presented because they have a large body of scientific evidence that supports them. These 6 standards were developed in such a manner to encourage students to analyze all forms of scientific evidence and draw their own conclusions.
Academic freedom legislation is in agreement with the spirit and purposes of South Dakota's science standards.
So what would academic freedom legislation actually accomplish? As I have written here previously, it would permit teachers to foster an environment of scientific inquiry by educating students about the evidence on both sides of scientific issues. Where this approach to learning has been adopted already, it trains students to think analytically. It awakens interest in science by inviting students to confront relevant research themselves. And students who succeed in science courses in grades K-12 are surely more likely to pursue degrees in those fields.
Inquiry in the classroom paves the way for inquiry in the lab. Contrary to what Mr. Anderson has been telling readers of the Argus Leader, enacting academic freedom legislation would have done a service to educational excellence in South Dakota.
Darwinism Vs. the real World XXVIII
Another Layer of Defense: The Adaptive Immune System:
Howard Glicksman February 9, 2016 11:19 AM
Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." Dr. Glicksman practices palliative medicine for a hospice organization.
The body is constantly under attack from powerful microorganisms that, if given the chance, will invade and take over. The body's first layer of defense is the skin and epithelium that lines the respiratory, gastrointestinal, and genitourinary tracts. If the microbes get past this barrier, they come up against the body's immune system. The immune system can be divided into the innate immune system,which each of us is born with and acts in the same way every time it encounters foreign matter, and the adaptive immune system which develops over time and reacts in a specific way to the foreign matter it is encountering.
Without the first layer of defense or both components of the immune system, our earliest ancestors could not have lived long enough to reproduce because they would have died from overwhelming infection. In the last several articles in this series, I have detailed how the cells and proteins of the innate immune system work. But on their own, they are incapable of defending the body from pathogenic microorganisms. Now we will start to look at the adaptive immune system, which brings extra intelligence, firepower, and precision accuracy to the field of battle to help the rest of the immune system get the job done.
The cells of the adaptive immune system are called lymphocytes and are produced in the bone marrow. The B-lymphocytes (B-cells) stay in the bone marrow to mature and the T-lymphocytes (T-cells) enter the blood and migrate to the thymus. The thymus is located inside the chest between the breastbone and the heart and is not to be confused with the thyroid gland, which is in the neck and secretes thyroid hormone. Once inside the thymus, the T-cells develop further and become subdivided into helper T-cells and cytotoxic T-cells. Since the lymphocytes come from the bone marrow and the thymus, these regions are known as primary lymphoid tissue.
Using about a thousand different receptors, each of the immune cells of the innate system can detect about a thousand different chemical patterns present on the surface of invading microbes. These cells activate when their receptors lock on to these foreign chemical patterns. Therefore, although the cells of the innate immune system can only detect a limited number of different chemical patterns, they all have the same ability to do so. This means that when they sense the presence of an intruder, all of the cells of the innate immune system can start to work together as a large fighting force.
In contrast, each lymphocyte has about a hundred thousand identical receptors on its surface, which can only detect a very small chemical pattern. This is usually just a few amino acids from within a very large protein molecule on the surface of a microbe. The first cells of the adaptive immune system to be understood were the B-cells. When B-cells activate by having their receptors lock on to these small chemical patterns on a microbe, they produce millions of specific proteins called antibodies.
Each of these antibodies has the same small chemical pattern as the specific receptors on the surface of the B-cell that produced it. Contact with one of these specific small chemical patterns on a microbe was responsible for generating specific antibodies from a B-cell, so scientists call them antigens. The word antigen is a shorthand term for an anti(body) gen(erating) small chemical pattern on a microbe which can cause an immune response from B-cells or T-cells. As opposed to the immune cells of the innate system, which can only detect about a thousand different chemical patterns, it is estimated that altogether, the cells of the adaptive immune system can detect about ten billion different antigens.
A lymphocyte activates when its specific receptors lock on to the specific antigens on the surface of a microbe. But, since each of the ten billion different lymphocytes can only detect one specific, small chemical pattern on a microbe, when they activate, there are too few of them around to provide an effective defense for the body. In other words, altogether, the cells of the adaptive immune system, with their ten billion different receptors, are much better at detecting foreign invasion than the innate immune system, with its one thousand receptors, but not as good at mounting an immediate response. The job of the adaptive immunity requires much more time than the one of innate immunity, because it must take the specific information it has detected about the pathogen, integrate it, and then use specific effector cells to bring about a more effective defense.
On its way back to the bloodstream, the fluid in the lymphatics travels through tissue that contains collections of lymphocytes. In this way, the lymphocytes are exposed to antigens from microbes that are present within the lymph that is draining all the organs and tissues of the body. These regions are called the secondary lymphoid tissue and consist of the lymph nodes, the spleen, the tonsils, and adenoids and the appendix. After they mature, lymphocytes migrate back and forth between the blood and the secondary lymphoid tissue, patrolling for foreign antigens.
Each helper T-cell has about a hundred thousand specific T-cell receptors on its surface that can detect only one specific antigen. Upon digestion of microbes in the tissues, dendritic cells and macrophages from the innate immune system migrate to the secondary lymphoid tissue. By placing some of the foreign protein they just digested on their surface, they present it to passing helper T-cells to activate them. Then the dendritic cells and macrophages release cytokines that enable the helper T-cells to grow and multiply into thousands of identical clones. This process converts the naïve helper T-cells into effector helper T-cells. These have no direct killing power, but regulate the immune response by releasing cytokines that attach to specific receptors on other immune cells to improve their killing ability and help them multiply.
Since there are only a limited number of cells in the adaptive immune system that can identify a specific microbe, it is important for them to be able to increase their population quickly in response to attack. In addition, some of the activated helper T-cells remain within the lymph nodes to act as memory cells so the immune system can respond faster the next time. The immune system demonstrates a measure of intelligence through helper T-cells. By knowing which specific reserves to multiply and mobilize in defending the body both during the present and future infection, it is able to adapt over time.
Just like the helper T-cell, the cytotoxic T-cell also has about a hundred thousand specific T-cell receptors on its surface that can detect only one specific antigen. After migrating to the secondary lymphoid tissue, dendritic cells that are infected with a virus or bacteria place foreign antigens on their surface so that a passing naive cytotoxic T-cell can attach to it and become activated. With the release of cytokines from either the dendritic cells or nearby helper T-cells that have responded to the same antigen, the cytotoxic T-cells grow and multiply into thousands of identical clones. The effector cytotoxic T-cells are now able to destroy any other host cell that has been infected by the same virus or bacteria. They use their specific receptors to identify and attach to the foreign antigens on their surface and then release deadly chemicals and enzymes to kill them and prevent the spreading of infection.
Like all lymphocytes, B-cells are made in the bone marrow, but unlike T-cells, they remain there to mature. Once released, they migrate back and forth between the secondary lymphoid tissue and the blood patrolling for antigens. Each B-cell has about a hundred thousand specific B -cell receptors on its plasma membrane that allow it to identify and attach to just one specific antigen. The molecular structure and shape of the part of the receptor that attaches to the antigen is identical to the antibodies the B-cell will produce when it activates. Unlike T-cells, B-cells do not need other cells to present them with antigens and when an antigen attaches to its specific receptors, it is brought into the B-cell.
The captured antigen is then processed and placed back onto the cells surface. When the now activated B-cell connects with an effector helper T-cell that has been activated by the same antigen, the latter releases cytokines that attach to receptors on the B-cell and stimulates it to multiply and become numerous identical plasma cells. Each of these plasma cells can produce millions of identical antibodies, shaped to react to the specific antigen that started the immune process in the first place. In addition, just like for the effector helper T-cells, some of the effector B-cells become memory cells that are stored in the secondary lymphoid tissue so the body can react faster the next time it becomes infected by the same microbe.
Just as a walled medieval town had to have enough defenders to prevent itself from invaders, so too, the body's immune system must have enough specific cells and proteins to protect itself from serious infection. We have seen that without the right amounts of each of the cells and proteins of the innate immune system, our earliest ancestors could not have survived long enough to reproduce. The blood must have at least 500 million helper T-cells per liter to be sure that there's enough help for cytotoxic T-cells to kill enough infected cells and for B-cells to produce millions of different antibodies which altogether can detect about ten billion different antigens. How do we know this? HIV.
HIV, or human immunodeficiency virus, targets helper T-cells and when chronic HIV infection causes their level in the blood to drop below 200 million per liter, the person is said to have AIDS (acquired immunodeficiency syndrome). A person with HIV-AIDS usually has not only severe infections caused by the usual pathogenic microbes, but also opportunistic infections. These infections usually do not cause infection in a person with normal immunity. HIV-AIDS can affect almost every organ system in the body and often results in the formation of different types of cancer as well. Having a helper T-cell blood count below 200 million per liter is not sufficient for allowing the adaptive immune system to do its job and is equivalent to not having enough defenders to help protect a walled medieval town from invasion and destruction. The result: usually death from overwhelming infection and sepsis.
Evolutionary biologists have imaginative theories about how the adaptive immune system came into being, but none of those really accounts for all of the irreducibly complex parts needed for it to work properly, nor the natural survival capacity needed to assure that there are enough of each of them to survive. Next time we will look at how the proteins of the adaptive immune system, the antibodies, work to provide the body's defense with additional intelligence, firepower, and precision accuracy.
Howard Glicksman February 9, 2016 11:19 AM
Editor's note: Physicians have a special place among the thinkers who have elaborated the argument for intelligent design. Perhaps that's because, more than evolutionary biologists, they are familiar with the challenges of maintaining a functioning complex system, the human body. With that in mind, Evolution News is delighted to offer this series, "The Designed Body." Dr. Glicksman practices palliative medicine for a hospice organization.
The body is constantly under attack from powerful microorganisms that, if given the chance, will invade and take over. The body's first layer of defense is the skin and epithelium that lines the respiratory, gastrointestinal, and genitourinary tracts. If the microbes get past this barrier, they come up against the body's immune system. The immune system can be divided into the innate immune system,which each of us is born with and acts in the same way every time it encounters foreign matter, and the adaptive immune system which develops over time and reacts in a specific way to the foreign matter it is encountering.
Without the first layer of defense or both components of the immune system, our earliest ancestors could not have lived long enough to reproduce because they would have died from overwhelming infection. In the last several articles in this series, I have detailed how the cells and proteins of the innate immune system work. But on their own, they are incapable of defending the body from pathogenic microorganisms. Now we will start to look at the adaptive immune system, which brings extra intelligence, firepower, and precision accuracy to the field of battle to help the rest of the immune system get the job done.
The cells of the adaptive immune system are called lymphocytes and are produced in the bone marrow. The B-lymphocytes (B-cells) stay in the bone marrow to mature and the T-lymphocytes (T-cells) enter the blood and migrate to the thymus. The thymus is located inside the chest between the breastbone and the heart and is not to be confused with the thyroid gland, which is in the neck and secretes thyroid hormone. Once inside the thymus, the T-cells develop further and become subdivided into helper T-cells and cytotoxic T-cells. Since the lymphocytes come from the bone marrow and the thymus, these regions are known as primary lymphoid tissue.
Using about a thousand different receptors, each of the immune cells of the innate system can detect about a thousand different chemical patterns present on the surface of invading microbes. These cells activate when their receptors lock on to these foreign chemical patterns. Therefore, although the cells of the innate immune system can only detect a limited number of different chemical patterns, they all have the same ability to do so. This means that when they sense the presence of an intruder, all of the cells of the innate immune system can start to work together as a large fighting force.
In contrast, each lymphocyte has about a hundred thousand identical receptors on its surface, which can only detect a very small chemical pattern. This is usually just a few amino acids from within a very large protein molecule on the surface of a microbe. The first cells of the adaptive immune system to be understood were the B-cells. When B-cells activate by having their receptors lock on to these small chemical patterns on a microbe, they produce millions of specific proteins called antibodies.
Each of these antibodies has the same small chemical pattern as the specific receptors on the surface of the B-cell that produced it. Contact with one of these specific small chemical patterns on a microbe was responsible for generating specific antibodies from a B-cell, so scientists call them antigens. The word antigen is a shorthand term for an anti(body) gen(erating) small chemical pattern on a microbe which can cause an immune response from B-cells or T-cells. As opposed to the immune cells of the innate system, which can only detect about a thousand different chemical patterns, it is estimated that altogether, the cells of the adaptive immune system can detect about ten billion different antigens.
A lymphocyte activates when its specific receptors lock on to the specific antigens on the surface of a microbe. But, since each of the ten billion different lymphocytes can only detect one specific, small chemical pattern on a microbe, when they activate, there are too few of them around to provide an effective defense for the body. In other words, altogether, the cells of the adaptive immune system, with their ten billion different receptors, are much better at detecting foreign invasion than the innate immune system, with its one thousand receptors, but not as good at mounting an immediate response. The job of the adaptive immunity requires much more time than the one of innate immunity, because it must take the specific information it has detected about the pathogen, integrate it, and then use specific effector cells to bring about a more effective defense.
On its way back to the bloodstream, the fluid in the lymphatics travels through tissue that contains collections of lymphocytes. In this way, the lymphocytes are exposed to antigens from microbes that are present within the lymph that is draining all the organs and tissues of the body. These regions are called the secondary lymphoid tissue and consist of the lymph nodes, the spleen, the tonsils, and adenoids and the appendix. After they mature, lymphocytes migrate back and forth between the blood and the secondary lymphoid tissue, patrolling for foreign antigens.
Each helper T-cell has about a hundred thousand specific T-cell receptors on its surface that can detect only one specific antigen. Upon digestion of microbes in the tissues, dendritic cells and macrophages from the innate immune system migrate to the secondary lymphoid tissue. By placing some of the foreign protein they just digested on their surface, they present it to passing helper T-cells to activate them. Then the dendritic cells and macrophages release cytokines that enable the helper T-cells to grow and multiply into thousands of identical clones. This process converts the naïve helper T-cells into effector helper T-cells. These have no direct killing power, but regulate the immune response by releasing cytokines that attach to specific receptors on other immune cells to improve their killing ability and help them multiply.
Since there are only a limited number of cells in the adaptive immune system that can identify a specific microbe, it is important for them to be able to increase their population quickly in response to attack. In addition, some of the activated helper T-cells remain within the lymph nodes to act as memory cells so the immune system can respond faster the next time. The immune system demonstrates a measure of intelligence through helper T-cells. By knowing which specific reserves to multiply and mobilize in defending the body both during the present and future infection, it is able to adapt over time.
Just like the helper T-cell, the cytotoxic T-cell also has about a hundred thousand specific T-cell receptors on its surface that can detect only one specific antigen. After migrating to the secondary lymphoid tissue, dendritic cells that are infected with a virus or bacteria place foreign antigens on their surface so that a passing naive cytotoxic T-cell can attach to it and become activated. With the release of cytokines from either the dendritic cells or nearby helper T-cells that have responded to the same antigen, the cytotoxic T-cells grow and multiply into thousands of identical clones. The effector cytotoxic T-cells are now able to destroy any other host cell that has been infected by the same virus or bacteria. They use their specific receptors to identify and attach to the foreign antigens on their surface and then release deadly chemicals and enzymes to kill them and prevent the spreading of infection.
Like all lymphocytes, B-cells are made in the bone marrow, but unlike T-cells, they remain there to mature. Once released, they migrate back and forth between the secondary lymphoid tissue and the blood patrolling for antigens. Each B-cell has about a hundred thousand specific B -cell receptors on its plasma membrane that allow it to identify and attach to just one specific antigen. The molecular structure and shape of the part of the receptor that attaches to the antigen is identical to the antibodies the B-cell will produce when it activates. Unlike T-cells, B-cells do not need other cells to present them with antigens and when an antigen attaches to its specific receptors, it is brought into the B-cell.
The captured antigen is then processed and placed back onto the cells surface. When the now activated B-cell connects with an effector helper T-cell that has been activated by the same antigen, the latter releases cytokines that attach to receptors on the B-cell and stimulates it to multiply and become numerous identical plasma cells. Each of these plasma cells can produce millions of identical antibodies, shaped to react to the specific antigen that started the immune process in the first place. In addition, just like for the effector helper T-cells, some of the effector B-cells become memory cells that are stored in the secondary lymphoid tissue so the body can react faster the next time it becomes infected by the same microbe.
Just as a walled medieval town had to have enough defenders to prevent itself from invaders, so too, the body's immune system must have enough specific cells and proteins to protect itself from serious infection. We have seen that without the right amounts of each of the cells and proteins of the innate immune system, our earliest ancestors could not have survived long enough to reproduce. The blood must have at least 500 million helper T-cells per liter to be sure that there's enough help for cytotoxic T-cells to kill enough infected cells and for B-cells to produce millions of different antibodies which altogether can detect about ten billion different antigens. How do we know this? HIV.
HIV, or human immunodeficiency virus, targets helper T-cells and when chronic HIV infection causes their level in the blood to drop below 200 million per liter, the person is said to have AIDS (acquired immunodeficiency syndrome). A person with HIV-AIDS usually has not only severe infections caused by the usual pathogenic microbes, but also opportunistic infections. These infections usually do not cause infection in a person with normal immunity. HIV-AIDS can affect almost every organ system in the body and often results in the formation of different types of cancer as well. Having a helper T-cell blood count below 200 million per liter is not sufficient for allowing the adaptive immune system to do its job and is equivalent to not having enough defenders to help protect a walled medieval town from invasion and destruction. The result: usually death from overwhelming infection and sepsis.
Evolutionary biologists have imaginative theories about how the adaptive immune system came into being, but none of those really accounts for all of the irreducibly complex parts needed for it to work properly, nor the natural survival capacity needed to assure that there are enough of each of them to survive. Next time we will look at how the proteins of the adaptive immune system, the antibodies, work to provide the body's defense with additional intelligence, firepower, and precision accuracy.
Yet more on human exceptionalism.
Dolphin Males Force Dolphin Females into Gang Intercourse
Wesley J. Smith February 8, 2016 2:46 PM
One of the distinctions separating humans from animals is that we are a species capable of morality. Only we create moral codes through rational means -- which is one reason they differ from society to society.
Animals are amoral. Whatever morality they appear to show -- often anthropomorphized by observers -- comes from instinct, not rational discourse or deliberation worked out and changeable over time.
With that in mind, dolphins are often romanticized as gentle sweethearts. But males force females into situations of gang forced intercourse, and may kill unrelated young. From the BBC story:
Small teams of males were usually part of larger "super-alliances" of up to 14 males.
It is also clear that the females are not particularly willing participants. "Male aggression toward a consort included chasing, hitting with the tail, head-jerks, charging, biting, or slamming bodily into the female," Connor and colleagues wrote in their 1992 paper.
The females frequently "bolted", but only managed to escape the males once in every four attempts. "Over the course of the year, a female will be herded by lots of different alliances over many different months," wrote Connor and colleagues
The males also apparently kill the young:
During 1996 and 1997, 37 young bottlenose dolphins washed up on beaches in Virginia. Superficially, there appeared to be nothing wrong with them, but necropsy revealed evidence of "severe blunt-force trauma".
The injuries were mainly to the head and chest, "and multiple rib fractures, lung lacerations, and soft tissue contusions were prominent," according to a study published in 2002. There was lots of evidence that adult dolphins were responsible for the deaths.
Notice, in the first instance, I didn't use the term "rape." That is because an animal cannot commit rape, which is a crime that involves moral turpitude. The same would apply to the term "murder."
The dolphins forcing themselves onto unwilling females, and killing the young, isn't wrong. It is merely dolphins being dolphins.
Of course, when humans do such things, they are judged rightly as monsters. That is because we are exceptional.
Wesley J. Smith February 8, 2016 2:46 PM
One of the distinctions separating humans from animals is that we are a species capable of morality. Only we create moral codes through rational means -- which is one reason they differ from society to society.
Animals are amoral. Whatever morality they appear to show -- often anthropomorphized by observers -- comes from instinct, not rational discourse or deliberation worked out and changeable over time.
With that in mind, dolphins are often romanticized as gentle sweethearts. But males force females into situations of gang forced intercourse, and may kill unrelated young. From the BBC story:
Small teams of males were usually part of larger "super-alliances" of up to 14 males.
It is also clear that the females are not particularly willing participants. "Male aggression toward a consort included chasing, hitting with the tail, head-jerks, charging, biting, or slamming bodily into the female," Connor and colleagues wrote in their 1992 paper.
The females frequently "bolted", but only managed to escape the males once in every four attempts. "Over the course of the year, a female will be herded by lots of different alliances over many different months," wrote Connor and colleagues
The males also apparently kill the young:
During 1996 and 1997, 37 young bottlenose dolphins washed up on beaches in Virginia. Superficially, there appeared to be nothing wrong with them, but necropsy revealed evidence of "severe blunt-force trauma".
The injuries were mainly to the head and chest, "and multiple rib fractures, lung lacerations, and soft tissue contusions were prominent," according to a study published in 2002. There was lots of evidence that adult dolphins were responsible for the deaths.
Notice, in the first instance, I didn't use the term "rape." That is because an animal cannot commit rape, which is a crime that involves moral turpitude. The same would apply to the term "murder."
The dolphins forcing themselves onto unwilling females, and killing the young, isn't wrong. It is merely dolphins being dolphins.
Of course, when humans do such things, they are judged rightly as monsters. That is because we are exceptional.
Monday 8 February 2016
Another failed Darwinian prediction VI
The molecular clock keeps evolutionary time:
In the 1960s molecular biologists learned how to analyze protein molecules and determine the sequence of amino acids that comprise a protein. It was then discovered that a given protein molecule varies somewhat from species to species. For example, hemoglobin, a blood protein, has similar function, overall size and structure in different species. But its amino acid sequence varies from species to species. Emile Zuckerkandl and Linus Pauling reasoned that if such sequence differences were the result of evolutionary change occurring over the history of life, then they could be used to estimate past speciation events—a notion that became known as the molecular clock. (Zuckerkandl and Pauling)
In later decades this concept of a molecular clock, relying on the assumption of a roughly constant rate of molecular evolution, became fundamental in evolutionary biology. (Thomas, et. al.) As the National Academy of Sciences explained, the molecular clock “determines evolutionary relationships among organisms, and it indicates the time in the past when species started to diverge from one another.” (Science and Creationism, 3) Indeed the molecular clock has been extolled as strong evidence for evolution and, in fact, a common sentiment has been that evolution was required to explain these evidences. As a leading molecular evolutionist wrote, the molecular clock is “only comprehensible within an evolutionary framework.” (Jukes, 119, emphasis in original)
The claim that the molecular clock can only be explained by evolution is, however, now a moot point as the mounting evidence shows that molecular differences often do not fit the expected pattern. The molecular clock which evolutionists had envisioned does not exist. The literature is full of instances where the molecular clock concept fails. For example, it was found early on that different types of proteins must evolve at very different rates if there is a molecular clock. For example the fibrinopeptide proteins in various species must have evolved more than five hundred times faster than the histone IV protein. Furthermore, it was found that the evolutionary rate of certain proteins must vary significantly over time, between different species, and between different lineages. (Thomas, et. al.; Andrews, 28)
The proteins relaxin, superoxide dismutase (SOD) and the glycerol-3-phosphate dehydrogenase (GPDH), for example, all contradict the molecular clock prediction. On the one hand, SOD unexpectedly shows much greater variation between similar types of fruit flies than it does between very different organisms such as animals and plants. On the other hand GPDH shows roughly the reverse trend for the same species. As one scientist concluded, GPDH and SOD taken together leave us “with no predictive power and no clock proper.” (Ayala)
Evolutionists are finding growing evidence that the purported rates of molecular evolution must vary considerably between species for a wide range of taxa, including mammals, arthropods, vascular plants, and even between closely related lineages. As one study concluded, “The false assumption of a molecular clock when reconstructing molecular phylogenies can result in incorrect topology and biased date estimation. … This study shows that there is significant rate variation in all phyla and most genes examined …” (Thomas, et. al.)
Evolutionists continue to use the molecular clock concept, but the many correction factors highlight the fact that the sequence data are being fit to the theory rather than the other way around. As one evolutionist warned, “It seems disconcerting that many exceptions exist to the orderly progression of species as determined by molecular homologies; so many in fact that I think the exception, the quirks, may carry the more important message.” (Schwabe)
References
Andrews, Peter. 1987. “Aspects of hominoid phylogeny” in Molecules and Morphology in Evolution, ed. Colin Patterson. Cambridge: Cambridge University Press.
Ayala, F. 1999. “Molecular clock mirages.” BioEssays 21:71-75.
Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.
Schwabe, C. 1986. “On the validity of molecular evolution.” Trends in Biochemical Sciences 11:280-282.
Science and Creationism: A View from the National Academy of Sciences. 2d ed. 1999. Washington, D.C.: National Academy Press.
Thomas, J. A., J. J. Welch, M. Woolfit, L. Bromham. 2006. “There is no universal molecular clock for invertebrates, but rate variation does not scale with body size.” Proceedings of the National Academy of Sciences 103:7366-7371.
Zuckerkandl, E., L. Pauling. 1965. “Molecules as documents of evolutionary history.” J Theoretical Biology 8:357-366.
In the 1960s molecular biologists learned how to analyze protein molecules and determine the sequence of amino acids that comprise a protein. It was then discovered that a given protein molecule varies somewhat from species to species. For example, hemoglobin, a blood protein, has similar function, overall size and structure in different species. But its amino acid sequence varies from species to species. Emile Zuckerkandl and Linus Pauling reasoned that if such sequence differences were the result of evolutionary change occurring over the history of life, then they could be used to estimate past speciation events—a notion that became known as the molecular clock. (Zuckerkandl and Pauling)
In later decades this concept of a molecular clock, relying on the assumption of a roughly constant rate of molecular evolution, became fundamental in evolutionary biology. (Thomas, et. al.) As the National Academy of Sciences explained, the molecular clock “determines evolutionary relationships among organisms, and it indicates the time in the past when species started to diverge from one another.” (Science and Creationism, 3) Indeed the molecular clock has been extolled as strong evidence for evolution and, in fact, a common sentiment has been that evolution was required to explain these evidences. As a leading molecular evolutionist wrote, the molecular clock is “only comprehensible within an evolutionary framework.” (Jukes, 119, emphasis in original)
The claim that the molecular clock can only be explained by evolution is, however, now a moot point as the mounting evidence shows that molecular differences often do not fit the expected pattern. The molecular clock which evolutionists had envisioned does not exist. The literature is full of instances where the molecular clock concept fails. For example, it was found early on that different types of proteins must evolve at very different rates if there is a molecular clock. For example the fibrinopeptide proteins in various species must have evolved more than five hundred times faster than the histone IV protein. Furthermore, it was found that the evolutionary rate of certain proteins must vary significantly over time, between different species, and between different lineages. (Thomas, et. al.; Andrews, 28)
The proteins relaxin, superoxide dismutase (SOD) and the glycerol-3-phosphate dehydrogenase (GPDH), for example, all contradict the molecular clock prediction. On the one hand, SOD unexpectedly shows much greater variation between similar types of fruit flies than it does between very different organisms such as animals and plants. On the other hand GPDH shows roughly the reverse trend for the same species. As one scientist concluded, GPDH and SOD taken together leave us “with no predictive power and no clock proper.” (Ayala)
Evolutionists are finding growing evidence that the purported rates of molecular evolution must vary considerably between species for a wide range of taxa, including mammals, arthropods, vascular plants, and even between closely related lineages. As one study concluded, “The false assumption of a molecular clock when reconstructing molecular phylogenies can result in incorrect topology and biased date estimation. … This study shows that there is significant rate variation in all phyla and most genes examined …” (Thomas, et. al.)
Evolutionists continue to use the molecular clock concept, but the many correction factors highlight the fact that the sequence data are being fit to the theory rather than the other way around. As one evolutionist warned, “It seems disconcerting that many exceptions exist to the orderly progression of species as determined by molecular homologies; so many in fact that I think the exception, the quirks, may carry the more important message.” (Schwabe)
References
Andrews, Peter. 1987. “Aspects of hominoid phylogeny” in Molecules and Morphology in Evolution, ed. Colin Patterson. Cambridge: Cambridge University Press.
Ayala, F. 1999. “Molecular clock mirages.” BioEssays 21:71-75.
Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.
Schwabe, C. 1986. “On the validity of molecular evolution.” Trends in Biochemical Sciences 11:280-282.
Science and Creationism: A View from the National Academy of Sciences. 2d ed. 1999. Washington, D.C.: National Academy Press.
Thomas, J. A., J. J. Welch, M. Woolfit, L. Bromham. 2006. “There is no universal molecular clock for invertebrates, but rate variation does not scale with body size.” Proceedings of the National Academy of Sciences 103:7366-7371.
Zuckerkandl, E., L. Pauling. 1965. “Molecules as documents of evolutionary history.” J Theoretical Biology 8:357-366.
Saturday 6 February 2016
Darwinism must fit into ever smaller gaps re:junk DNA
Junk DNA: Is Preventing Breast Cancer a Function?
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
Evolution News & Views February 6, 2016 4:33 AM
Each time a function is found for a piece of non-coding DNA, the "junk DNA" myth gets more mythological. Here's a function that has been revealed for a certain long, non-coding transcript of DNA into RNA (lncRNA). It helps prevent breast cancer and ovarian cancer.
Researchers at the University of Bath explain why it is difficult to find these functions for non-coding parts of the genome:
The human genome contains around three metres of DNA, of which only about two per cent contains genes that code for proteins. Since the sequencing of the complete human genome in 2000, scientists have puzzled over the role of the remaining 98 per cent.
In recent years it has become apparent that a lot of this non-coding DNA is actually transcribed into non-coding RNA. However, there is still a debate as to whether non-coding RNA is just 'noise' or whether it serves any function in the cell.
Part of the reason for this uncertainty is that it is very difficult to knock-out non-coding RNA without damaging the DNA, which can lead to off-target effects and false results.
They are clearly aware of the "debate" about junk DNA and the results of ENCODE that found that the majority of the genome is actually transcribed (they referenced ENCODE in the paper). As we have reported often, some members of the evolution side of the debate expect most of the DNA is junk. The design side expects that much of it (but not necessarily all) is functional. Thanks to this research, we have a new case that may point the way to future discoveries.
The news release is titled, "'Junk' DNA plays role in preventing breast cancer." It's based on an open-access paper in Nature Communications. Most readers scanning the paper will see what researchers are up against. Discussion of the complex interactions of parts -- lncRNAs transcripts, small interfering RNAs (siRNAs), promoters, exons, introns, alleles, interference in cis and trans and all the rest -- gets into the technical weeds fast. Thankfully, the release simplifies the essence of the finding. Basically, a piece of non-coding DNA "keeps cells healthy" by preventing a genetic "switch" from getting stuck.
Dr Adele Murrell, from the University of Bath's Department of Biology & Biochemistry, led the study. She explained: "The number of cells in our body are balanced by the level at which cells replicate and replace the ones that die. Sometimes the switches that control this growth get stuck in the 'on' position, which can lead to cancer.
"As the tumour grows and the cancer cells get crowded, they start to break away from the tumour, change shape and are able to burrow through tissues to the bloodstream where they migrate to other parts of the body, which is how the cancer spreads. This process is called metastasis and requires a whole network of genes to regulate the transformation of cell shape and mobilisation.
Dr Lovorka Stojic, from Cancer Research UK Cambridge Institute, the first author of this work identified that GNG12-AS1, a strand of non-coding RNA, prevents the growth switch getting stuck and suppresses metastasis. The specific genomic region where this non-coding RNA is located often gets damaged in breast cancer patients -- this control is removed and the cancer cells spread.
The researchers found that the lncRNA GNG12-AS1 acts as a molecular "rheostat" (their term) that controls the expression of an adjacent gene, DIRAS3, a tumor suppressor. It does it by two mechanisms. One is by regulating the number of transcripts of the tumor suppressor. But if that gets out of control, it can even suppress the "network of genes that prepare cells to change their shape and prepare for metastasis."
By experimentally reducing the amount of GNG12-AS1 produced, either by preventing its transcription or destroying the transcripts, they found that cells start becoming cancerous. This explains why in cancer patients, the switch is stuck:
DIRAS3 is downregulated in 70% of breast and ovarian cancer, and its loss of expression correlates with cancer progression and metastasis. The mechanism responsible for DIRAS3 downregulation to date involves different epigenetic mechanisms and loss of heterozygosity. We hypothesized that TI [transcriptional interference] by GNG12-AS1 could represent an additional layer of regulating DIRAS3 dosage.
The interactions are far more complex than can be described here. Suffice it to say that this long non-coding RNA, which would have been considered "junk" previously, plays a crucial role in regulating the amount of an important tumor suppressor gene. It's a "stable lncRNA localized in the nucleus" with a half-life of 20 to 25 hours, meaning it needs to be transcribed often. Other processes regulate the amount of the lncRNA in a very complex choreography of enhancers, suppressors, and feedback loops. Levels of expression also vary depending on the tissue involved.
It has become increasingly clear that non-coding parts of the genome play vital roles in regulating the coding parts. Regulation is an important function. A system that generates parts without regard to the amount needed is a system out of control. How cool is it to find a code that codes for products that regulate the amount of products in other parts of the code? Not only do we see function emerging for the non-coding regions, we see design on a more colossal scale than anyone could have imagined.
The University of Bath is an internationally recognized center of excellence in biological research. It's encouraging to see their biologists actively challenging the "junk DNA" myth:
Dr Kat Arney, science communication manager at Cancer Research UK, said: "Only a tiny fraction of our DNA contains actual genes, and we know that at least some of the bits in between -- often dismissed as 'junk' -- play important roles in controlling how genes get switched on and off at the right time and in the right place.
When the Human Genome project found that only 2 percent of the genome coded for proteins, the right question should have been, "What is all the rest doing?" Some evolutionists were too quick to dismiss it as a pile of useless leftovers from time and chance. Cancer patients around the world can be grateful that these researchers didn't buy that explanation, but looked beyond the unknown for greater understanding.
"Research like this is helping is to unpick the precise details about how these regions work, shedding light on their potential role in the development [or prevention] of cancer and pointing towards new approaches for tackling the disease."
If a system works, it's not happening by accident. That's the intelligent-design spirit that promises to shed more light into the genomic black box.
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