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Thursday 22 June 2017
On junk science re:junk DNA.
Jonathan Wells: Zombie Science Keeps Pushing Junk DNA Myth
David Klinghoffer | @d_klinghoffer
The idea that a vast majority of our DNA is “junk,” an evolutionary relic, was just what evolutionists expected. It made sense. Darwin advocates such as Jerry Coyne and Francis Collins advanced it as proof for their claims. Alas for them, it turned out not to be true.
In a video conversation, Zombie Science author Jonathan Wells explains how the “Junk DNA” narrative was overturned by good science, including but far from limited to the ENCODE project. Did evolutionary diehards accept this? No! See it here:
If you follow the scientific literature, new functions for “junk” turn up on an almost weekly basis. But the diehards keep insisting on the myth. They strenuously resist a growing body of evidence. Why? Because as Dr. Wells clarifies, evolution for them is not an ordinary scientific theory. It’s a fixed idea. It is an ideology that must be true “no matter what.”
So how evidence is interpreted is wrenched into line with the ideology. And this is what we mean by “zombie science.” Watch and enjoy.
David Klinghoffer | @d_klinghoffer
The idea that a vast majority of our DNA is “junk,” an evolutionary relic, was just what evolutionists expected. It made sense. Darwin advocates such as Jerry Coyne and Francis Collins advanced it as proof for their claims. Alas for them, it turned out not to be true.
In a video conversation, Zombie Science author Jonathan Wells explains how the “Junk DNA” narrative was overturned by good science, including but far from limited to the ENCODE project. Did evolutionary diehards accept this? No! See it here:
If you follow the scientific literature, new functions for “junk” turn up on an almost weekly basis. But the diehards keep insisting on the myth. They strenuously resist a growing body of evidence. Why? Because as Dr. Wells clarifies, evolution for them is not an ordinary scientific theory. It’s a fixed idea. It is an ideology that must be true “no matter what.”
So how evidence is interpreted is wrenched into line with the ideology. And this is what we mean by “zombie science.” Watch and enjoy.
Yet more on the chasm between life and everything else.
“Life Is a Discontinuity in the Universe”
David Klinghoffer | @d_klinghoffer
David Klinghoffer | @d_klinghoffer
In a really excellent new ID the Future episode with Todd Butterfield, Steve Laufmann puts the engineering challenge to gradualist evolutionary schemes about as powerfully as one could do. An enterprise architecture consultant, he is a most gifted and entertaining explainer.
There are 37 trillion cells in the human body, some 200 cell types, and 12,000+ specialized proteins. How does it all come together? In human ontogenesis, a 9-month process “turns a zygote into what I call a tax deduction,” says Laufmann. Building a system like this that “leaps together at the same time to create us” (as Butterfield puts it) is the most stunning engineering feat ever accomplished as far as we know.
The discussion features one memorable phrasing after another. “Life is a discontinuity in the universe,” and explaining it means explaining the property of “coherence” associated with engineered systems. Darwinian theory proposes that this was accomplished through random changes gradually accumulating. That entails maintaining “an adaptive continuum” of life where “any causal mechanism that’s proposed has to be able to produce all the changes for every discrete step within one generation.” In this way, unguided evolution could accomplish trivial changes – on the order of skin color, the shape of the nose or the earlobe – but “basics” (how a spleen functions, for example) are quite outside the range.
For the Darwin proponent, it looks hopeless. Laufmann: “Random changes only make the impossible even more impossible. It’s like the impossible squared. It just can’t happen.”
Taking all of this together, what you expect, rather than gradual change as evolutionists picture it, is sudden explosions of complexity. And this is just what the fossil record shows.
It’s a wonderful and enlightening conversation, demonstrating again the necessity of introducing the engineer’s perspective in any realistic estimation of how evolution could work. Darwin proponents almost never seem to consider these challenges. Listen to the podcast here, or download it here.
Tuesday 20 June 2017
Are 'orphaned genes' a thing?
A Reader Asks, "Are De Novo Genes Real?"
Ann Gauger
We get good questions here at Evolution News. (Give us yours by hitting the orange Email Us button at the top of the page.) Today, a reader writes to ask, "Are de novo genes real?" This is a question that touches on a number of topics relevant to evolutionary biology, dealing with one of the most exciting aspects of genomic research today. So what are these things called de novo genes?
De novo genes are genes that are present in a particular species or taxonomic group, and not present in any others. Why are they there and where did they come from? To answer these questions we have to first deal with some important assumptions of evolutionary biology.
The first assumption is that sibling species are the product of descent with modification. The evidence cited in favor of this idea is that there is similarity of DNA sequence between sibling species, and that organisms can be grouped in nested hierarchies based on sequence comparisons. Now this hypothesis of common descent may be right. However, there are unresolved contradictions in the literature. So common descent is not unequivocally proven. De novo genes are one of those challenges to common descent. Let me explain why.
De novo genes, new genes present in one taxonomic group but not in others, are sometimes called orphan genes because they have no parent genes. They are also called taxonomically restricted genes (TRGs), because they may be shared by closely related species of the same taxon, but not others. What's a taxon? It's a level of classification, such as species, genus, family, order, class or phylum. Species of the same genus, for example, may share genes in common that are missing from all other species.
Because the field of research is still developing, different research groups use different criteria for deciding what counts as a TRG. For example, one recent estimate says that there are 634 genes that appear to have arisen de novo in the human genome, as compared with the chimpanzee and macaque genomes. But they counted RNA transcripts as genes, even if they have not yet been shown to code for protein. Another older estimate of over a thousand transcripts was finally reduced to a much lower number of de novo genes, because the researchers ruled out almost all of those candidate genes as non-protein coding. For a discussion about why this is, go here.
Despite these disagreements, de novo genes do exist. But when their origin -- where they came from -- is discussed, it reveals yet another assumption of evolutionary biologists. Evolutionists say, "Look, these orphan genes arose de novo. We can see how they might have been spliced together from similar DNA present elsewhere in the genome, or they might have come from non-coding DNA that has acquired a promoter or transcription factor binding site, and so is now expressed, and makes a functional protein, in the right place and at the right time."
These sentences reveal the second assumption -- that the existence of these new genes indicates there are natural processes to make them. After all, it must be possible to splice or activate new sequences to make TRGs, because there are TRGs.
That's an assumption of naturalism. The problem is there is no evidence to show that those proposed mechanisms actually work. There are no experiments that I know of to demonstrate that splicing yields functional products. Attempts in the lab show that splicing together even related protein domains yields non-functional products. Also, no one has shown that it is easy to acquire a promoter or transcription factor binding site so as to turn inactive, non-coding DNA into expressed, functional DNA. Getting a functional protein from random non-coding sequence is impossibly hard and would have to be demonstrated. If the function is regulating other genes via RNA, that would have to be proven to be feasible, too.
So do we know where TRGs came from? If no one tests how hard it is to splice together random sequence and get functional stuff, or how hard it is to acquire a new promoter, then we don't know whether de novo genes can be developed by evolutionary processes. If not, the alternative is shocking to evolutionary biologists -- perhaps, just perhaps they were made by a designer for that particular species or group. Perhaps the non-coding DNA was already ready to be functional, like an actor waiting in the wings for his cue, and was only activated in that one particular taxonomic group.
Bear in mind that TRGs can be up to 10-20 percent of a taxonomic group's genome, and may encode many of the special proteins unique to that taxonomic group. That's a huge chunk of DNA to arise by natural processes alone, and a big challenge for common descent. I am thinking of the phylum Cnidaria here. All Cnidaria (sea anemones, jelly fish, and Hydra for example) have tentacles with specialized cells called cnidocytes or nematocysts, which eject a little barbed tubule with a toxin into whatever touches them. They use these cells to capture and immobilize their prey. Many of the specialized proteins needed to make the nematocysts are TRGs specific to the phylum Cnidaria. Cnidaria are among the oldest of all extant phyla. Was their origin unique?
Take home lesson: Are de novo genes real? Yes. Do we know where they came from? No. Do they say something important about evolutionary processes? Indeed. But what they say remains to be seen.
Ann Gauger
We get good questions here at Evolution News. (Give us yours by hitting the orange Email Us button at the top of the page.) Today, a reader writes to ask, "Are de novo genes real?" This is a question that touches on a number of topics relevant to evolutionary biology, dealing with one of the most exciting aspects of genomic research today. So what are these things called de novo genes?
De novo genes are genes that are present in a particular species or taxonomic group, and not present in any others. Why are they there and where did they come from? To answer these questions we have to first deal with some important assumptions of evolutionary biology.
The first assumption is that sibling species are the product of descent with modification. The evidence cited in favor of this idea is that there is similarity of DNA sequence between sibling species, and that organisms can be grouped in nested hierarchies based on sequence comparisons. Now this hypothesis of common descent may be right. However, there are unresolved contradictions in the literature. So common descent is not unequivocally proven. De novo genes are one of those challenges to common descent. Let me explain why.
De novo genes, new genes present in one taxonomic group but not in others, are sometimes called orphan genes because they have no parent genes. They are also called taxonomically restricted genes (TRGs), because they may be shared by closely related species of the same taxon, but not others. What's a taxon? It's a level of classification, such as species, genus, family, order, class or phylum. Species of the same genus, for example, may share genes in common that are missing from all other species.
Because the field of research is still developing, different research groups use different criteria for deciding what counts as a TRG. For example, one recent estimate says that there are 634 genes that appear to have arisen de novo in the human genome, as compared with the chimpanzee and macaque genomes. But they counted RNA transcripts as genes, even if they have not yet been shown to code for protein. Another older estimate of over a thousand transcripts was finally reduced to a much lower number of de novo genes, because the researchers ruled out almost all of those candidate genes as non-protein coding. For a discussion about why this is, go here.
Despite these disagreements, de novo genes do exist. But when their origin -- where they came from -- is discussed, it reveals yet another assumption of evolutionary biologists. Evolutionists say, "Look, these orphan genes arose de novo. We can see how they might have been spliced together from similar DNA present elsewhere in the genome, or they might have come from non-coding DNA that has acquired a promoter or transcription factor binding site, and so is now expressed, and makes a functional protein, in the right place and at the right time."
These sentences reveal the second assumption -- that the existence of these new genes indicates there are natural processes to make them. After all, it must be possible to splice or activate new sequences to make TRGs, because there are TRGs.
That's an assumption of naturalism. The problem is there is no evidence to show that those proposed mechanisms actually work. There are no experiments that I know of to demonstrate that splicing yields functional products. Attempts in the lab show that splicing together even related protein domains yields non-functional products. Also, no one has shown that it is easy to acquire a promoter or transcription factor binding site so as to turn inactive, non-coding DNA into expressed, functional DNA. Getting a functional protein from random non-coding sequence is impossibly hard and would have to be demonstrated. If the function is regulating other genes via RNA, that would have to be proven to be feasible, too.
So do we know where TRGs came from? If no one tests how hard it is to splice together random sequence and get functional stuff, or how hard it is to acquire a new promoter, then we don't know whether de novo genes can be developed by evolutionary processes. If not, the alternative is shocking to evolutionary biologists -- perhaps, just perhaps they were made by a designer for that particular species or group. Perhaps the non-coding DNA was already ready to be functional, like an actor waiting in the wings for his cue, and was only activated in that one particular taxonomic group.
Bear in mind that TRGs can be up to 10-20 percent of a taxonomic group's genome, and may encode many of the special proteins unique to that taxonomic group. That's a huge chunk of DNA to arise by natural processes alone, and a big challenge for common descent. I am thinking of the phylum Cnidaria here. All Cnidaria (sea anemones, jelly fish, and Hydra for example) have tentacles with specialized cells called cnidocytes or nematocysts, which eject a little barbed tubule with a toxin into whatever touches them. They use these cells to capture and immobilize their prey. Many of the specialized proteins needed to make the nematocysts are TRGs specific to the phylum Cnidaria. Cnidaria are among the oldest of all extant phyla. Was their origin unique?
Take home lesson: Are de novo genes real? Yes. Do we know where they came from? No. Do they say something important about evolutionary processes? Indeed. But what they say remains to be seen.
Between physics and abiogenesis an unbridgeable chasm?
The Origin of Life, Self-Organization, and Information
Brian Miller
Brian Miller
In an article here yesterday, I described the thermodynamic challenges to any purely materialistic theory for the origin of life. Now, I will address one of the most popular and misunderstood claims that the first cell emerged through a process that demonstrated the property known as self-organization.
As I mentioned in the previous article, origin-of-life researchers often argue that life developed in an environment that was driven far from equilibrium, often referred to as a non-equilibrium dissipative system. In such systems, energy and/or mass constantly enters and leaves, and this flow spontaneously generates “order” such as the roll patterns in boiling water, the funnel of a tornado, or wave patterns in the Belousov-Zhabotinsky reaction. The assertion is that some analogous type of self-organizational process could have created the order in the first cell. Such claims sound reasonable at first, but they completely break down when the differences between self-organizational order and cellular order are examined in detail. Instead, the origin of life required complex cellular machinery and preexisting sources of information.
The main reason for the differences between self-organizational and cellular order is that the driving tendencies in non-equilibrium systems move in the opposite direction to what is needed for both the origin and maintenance of life. First, all realistic experiments on the genesis of life’s building blocks produce most of the needed molecules in very small concentrations, if at all. And, they are mixed together with contaminants, which would hinder the next stages of cell formation. Nature would have needed to spontaneously concentrate and purify life’s precursors. However, the natural tendency would have been for them to diffuse and to mix with other chemicals, particularly in such environments as the bottom of the ocean.
Concentration of some of life’s precursors could have taken place in an evaporating pool, but the contamination problem would then become much worse since precursors would be greatly outnumbered by contaminants. Moreover, the next stages of forming a cell would require the concentrated chemicals to dissolve back into some larger body of water, since different precursors would have had to form in different locations with starkly different initial conditions. In his book on Origins, Robert Shapiro described these details in relation to the exquisite orchestration required to produce life.
In addition, many of life’s building blocks come in both right and left-handed versions, which are mirror opposites. Both forms are produced in all realistic experiments in equal proportions, but life can only use one of them: in today’s life, left-handed amino acids and right-handed sugars. The origin of life would have required one form to become increasingly dominant, but nature would drive a mixture of the two forms toward equal percentages, the opposite direction. As a related but more general challenge, all spontaneous chemical reactions move downhill toward lower free energy. However, a large portion of the needed reactions in the origin and maintenance of life move uphill toward higher free energy. Even those that move downhill typically proceed too slowly to be useful. Nature would have had to reverse most of its natural tendencies in any scenario for extended periods of time. Scientists have never observed any such event at any time in the history of the universe.
These challenges taken together help clarify the dramatic differences between the two types of order:
Self-organizational processes create order (i.e. funnel cloud) at the macroscopic (visible) level, but they generate entropy at the microscopic level. In contrast, life requires the entropy at the cellular size scale to decrease.
Self-organizational patterns are driven by processes which move toward lower free energy. Many processes which generate cellular order move toward higher free energy.
Self-organizational order is dynamic — material is in motion and the patterns are changing over time. The cellular order is static — molecules are in fixed configurations, such as the sequence of nucleotides in DNA or the structure of cellular machines.
Self-organizational order is driven by natural laws. The order in cells represents specified complexity — molecules take on highly improbable arrangements which are not the product of natural processes but instead are arranged to achieve functional goals.
These differences demonstrate that self-organizational processes could not have produced the order in the first cell. Instead, cellular order required molecular machinery to process energy from outside sources and to store it in easily accessible repositories. And, it needed information to direct the use of that energy toward properly organizing and maintaining the cell.
A simple analogy will demonstrate why machinery and information were essential. Scientists often claim that any ancient energy source could have provided the needed free energy to generate life. However, this claim is like a couple returning home from a long vacation to find that their children left their house in complete disarray, with clothes on the floor, unwashed dishes in the sink, and papers scattered across all of the desks. The couple recently heard an origin-of-life researcher claim that order could be produced for free from any generic source of energy. Based on this idea, they pour gasoline on their furniture and then set it on fire. They assume that the energy released from the fire will organize their house. However, they soon realize that unprocessed energy creates an even greater mess.
Based on this experience, the couple instead purchase a solar powered robot. The solar cells process the energy from the sun and convert it into useful work. But, to the couple’s disappointment the robot then starts throwing objects in all directions. They look more closely at the owner’s manual and realize they need to program the robot with instructions on how to perform the desired tasks to properly clean up the house.
In the same way, the simplest cell required machinery, such as some ancient equivalent to ATP synthase or chloroplasts, to process basic chemicals or sunlight. It also needed proteins with the proper information contained in their amino acid sequences to fold into other essential cellular structures, such as portals in the cell membrane. And, it needed proteins with the proper sequences to fold into enzymes to drive the metabolism. A key role of the enzymes is to link reactions moving toward lower free energy (e.g. ATP → ADP + P) to reactions, such as combining amino acids into long chains, which go uphill. The energy from the former can then be used to drive the latter, since the net change in free energy is negative. The free-energy barrier is thus overcome.
However, the energy-processing machinery and information-rich proteins were still not enough. Proteins eventually break down, and they cannot self-replicate. Additional machinery was also needed to constantly produce new protein replacements. Also, the proteins’ sequence information had to have been stored in DNA using some genetic code, where each amino acid was represented by a series of three nucleotides know as a codon in the same way English letters are represented in Morse Code by dots and dashes. However, no identifiable physical connection exists between individual amino acids and their respective codons. In particular, no amino acid (e.g., valine) is much more strongly attracted to any particular codon (e.g., GTT) than to any other. Without such a physical connection, no purely materialistic process could plausibly explain how amino acid sequences were encoded into DNA. Therefore, the same information in proteins and in DNA must have been encoded separately.
In addition, the information in DNA is decoded back into proteins through the use of ribosomes, tRNAs, and special enzymes called aminoacyl tRNA sythetases (aaRS). The aaRSs bind the correct amino acids to the correct tRNAs associated with the correct codons, so these enzymes contain the decoding key in their 3D structures. All life uses this same process, so the first cell almost certainly functioned similarly. However, no possible connection could exist between the encoding and the decoding processes, since the aaRSs’ structures are a result of their amino acid sequences, which happen to be part of the information encoded in the DNA. Therefore, the decoding had to have developed independently of the encoding, but they had to use the same code. And, they had to originate at the same time, since each is useless without the other.
All of these facts indicate that the code and the sequence information in proteins/DNA preexisted the original cell. And, the only place that they could exist outside of a physical medium is in a mind, which points to design.
Monday 19 June 2017
Actually,it is rocket science.
Rocket Science in a Microbe Saves the Planet
Evolution News & Views
Anammox. It's a good term to learn. Wikipedia's first paragraph stresses its importance:
Anammox, an abbreviation for ANaerobic AMMonium OXidation, is a globally important microbial process of the nitrogen cycle. The bacteria mediating this process were identified in 1999, and at the time were a great surprise for the scientific community. It takes place in many natural environments... [Emphasis added.]
And now, the news. A team of European scientists found something very interesting about the bacteria. Publishing in Nature, the researchers tell how they have ascertained the structure of a molecular machine that performs chemical wizardry using rocket science.
Anaerobic ammonium oxidation (anammox) has a major role in the Earth's nitrogen cycle and is used in energy-efficient wastewater treatment. This bacterial process combines nitrite and ammonium to form dinitrogen (N2) gas, and has been estimated to synthesize up to 50% of the dinitrogen gas emitted into our atmosphere from the oceans. Strikingly, the anammox process relies on the highly unusual, extremely reactive intermediate hydrazine, a compound also used as a rocket fuel because of its high reducing power. So far, the enzymatic mechanism by which hydrazine is synthesized is unknown. Here we report the 2.7 Å resolution crystal structure, as well as biophysical and spectroscopic studies, of a hydrazine synthase multiprotein complex isolated from the anammox organism Kuenenia stuttgartiensis. The structure shows an elongated dimer of heterotrimers, each of which has two unique c-type haem-containing active sites, as well as an interaction point for a redox partner. Furthermore, a system of tunnels connects these active sites. The crystal structure implies a two-step mechanism for hydrazine synthesis: a three-electron reduction of nitric oxide to hydroxylamine at the active site of the γ-subunit and its subsequent condensation with ammonia, yielding hydrazine in the active centre of the α-subunit. Our results provide the first, to our knowledge, detailed structural insight into the mechanism of biological hydrazine synthesis, which is of major significance for our understanding of the conversion of nitrogenous compounds in nature.
Dinitrogen gas (N2) is a tough nut to crack. The atoms pair up with a triple bond, very difficult for humans to break without a lot of heat and pressure. Fortunately, this makes it very inert for the atmosphere, but life needs to get at it to make amino acids, muscles, organs, and more. Nitrogenase enzymes in some microbes, such as soil bacteria, are able break apart the atoms at ambient temperatures (a secret agricultural chemists would love to learn). They then "fix" nitrogen into compounds such as ammonia (NH3) that can be utilized by plants and the animals that eat them. To have a nitrogen cycle, though, something has to return the N2 gas back to the atmosphere. That's the job of anammox bacteria.
Most nitrogen on earth occurs as gaseous N2 (nitrogen oxidation number 0). To make nitrogen available for biochemical reactions, the inert N2 has to be converted to ammonia (oxidation number −III), which can then be assimilated to produce organic nitrogen compounds, or be oxidized to nitrite (oxidation number +III) or nitrate (+V). The reduction of nitrite in turn results in the regeneration of N2, thus closing the biological nitrogen cycle.
Let's take a look at the enzyme that does this, the "hydrazine synthase multiprotein complex." Rocket fuel; imagine! No wonder the scientific community was surprised. The formula for hydrazine is N2H4. It's commonly used to power thrusters on spacecraft, such as the Cassini Saturn orbiter and the New Horizons probe that went by Pluto recently. Obviously, the anammox bacteria must handle this highly reactive compound with great care. Here's their overview of the reaction sequence. Notice how the bacterium gets some added benefit from its chemistry lab:
Our current understanding of the anammox reaction (equation (1)) is based on genomic, physiological and biochemical studies on the anammox bacterium K. stuttgartiensis. First, nitrite is reduced to nitric oxide (NO, equation (2)), which is then condensed with ammonium-derived ammonia (NH3) to yield hydrazine (N2H4, equation (3)). Hydrazine itself is a highly unusual metabolic intermediate, as it is extremely reactive and therefore toxic, and has a very low redox potential (E0′ = −750 mV). In the final step in the anammox process, it is oxidized to N2, yielding four electrons (equation (4)) that replenish those needed for nitrite reduction and hydrazine synthesis and are used to establish a proton-motive force across the membrane of the anammox organelle, the anammoxosome, driving ATP synthesis.
We've discussed ATP synthase before. It's that rotary engine in all life that runs on proton motive force. Here, we see that some of the protons needed for ATP synthesis come from the hydrazine reaction machine. Cool!
What does the anammox enzyme look like? They say it has tunnels between the active sites. The "hydrazine synthase" module is "biochemically unique." Don't look for a common ancestor, in other words. It's part of a "tightly coupled multicomponent system" they determined when they lysed a cell and watched its reactivity plummet. Sounds like an irreducibly complex system.
The paper's diagrams of hydrazine synthase (HZS) show multiple protein domains joined in a "crescent-shaped dimer of heterotrimers" labeled alpha, beta, and gamma, constituted in pairs. The machine also contains multiple haem units (like those in hemoglobin, but unique) and "one zinc ion, as well as several calcium ions." Good thing those atoms are available in Earth's crust.
Part of the machine looks like a six-bladed propeller. Another part has seven blades. How does it work? Everything is coordinated to carefully transfer electrons around. This means that charge distributions are highly controlled for redox (reduction-oxidation) reactions (i.e., those that receive or donate electrons). The choice of adverbs shows that their eyes were lighting up at their first view of this amazing machine. Note how emotion seasons the jargon:
Intriguingly, our crystal structure revealed a tunnel connecting the haem αI and γI sites (Fig. 3a). This tunnel branches off towards the surface of the protein approximately halfway between the haem sites, making them accessible to substrates from the solvent. Indeed, binding studies show that haem αI is accessible to xenon (Extended Data Fig. 4c). Interestingly, in-between the α- and γ-subunits, the tunnel is approached by a 15-amino-acid-long loop of the β-subunit (β245-260), placing the conserved βGlu253, which binds a magnesium ion, into the tunnel.
We would need to make another animation to show the machine in action, but here's a brief description of how it works. The two active sites, connected by a tunnel, appear to work in sequence. HZS gets electrons from cytochrome c, a well-known enzyme. The electrons enter the machine through one of the haem units, where a specifically-placed gamma unit adds protons. A "cluster of buried polar residues" transfers protons to the active center of the gamma subunit. A molecule named hydroxylamine (H3NO) diffuses into the active site, assisted by the beta subunit. It binds to another haem, which carefully positions it so that it is "bound in a tight, very hydrophobic pocket, so that there is little electrostatic shielding of the partial positive charge on the nitrogen." Ammonia then comes in to do a "nucleophilic attack" on the nitrogen of the molecule, yielding hydrazine. The hydrazine is then in position to escape via the tunnel branch leading to the surface. Once they determined this sequence, a light went on:
Interestingly, the proposed scheme is analogous to the Raschig process used in industrial hydrazine synthesis. There, ammonia is oxidized to chloramine (NH2Cl, nitrogen oxidation number −I, like in hydroxylamine), which then undergoes comproportionation with another molecule of ammonia to yield hydrazine.
(But that, we all know, is done by intelligent design.)
So here's something you can meditate on when you take in another breath. The nitrogen gas that comes into your lungs is a byproduct of an exquisitely designed, precision nanomachine that knows a lot about organic redox chemistry and safe handling of rocket fuel. This little machine, which also knows how to recycle and reuse all its parts in a sustainable "green" way, keeps the nitrogen in balance for the whole planet. Intriguing. Interesting. As Mr. Spock might say, fascinating.
Evolution News & Views
Anammox. It's a good term to learn. Wikipedia's first paragraph stresses its importance:
Anammox, an abbreviation for ANaerobic AMMonium OXidation, is a globally important microbial process of the nitrogen cycle. The bacteria mediating this process were identified in 1999, and at the time were a great surprise for the scientific community. It takes place in many natural environments... [Emphasis added.]
And now, the news. A team of European scientists found something very interesting about the bacteria. Publishing in Nature, the researchers tell how they have ascertained the structure of a molecular machine that performs chemical wizardry using rocket science.
Anaerobic ammonium oxidation (anammox) has a major role in the Earth's nitrogen cycle and is used in energy-efficient wastewater treatment. This bacterial process combines nitrite and ammonium to form dinitrogen (N2) gas, and has been estimated to synthesize up to 50% of the dinitrogen gas emitted into our atmosphere from the oceans. Strikingly, the anammox process relies on the highly unusual, extremely reactive intermediate hydrazine, a compound also used as a rocket fuel because of its high reducing power. So far, the enzymatic mechanism by which hydrazine is synthesized is unknown. Here we report the 2.7 Å resolution crystal structure, as well as biophysical and spectroscopic studies, of a hydrazine synthase multiprotein complex isolated from the anammox organism Kuenenia stuttgartiensis. The structure shows an elongated dimer of heterotrimers, each of which has two unique c-type haem-containing active sites, as well as an interaction point for a redox partner. Furthermore, a system of tunnels connects these active sites. The crystal structure implies a two-step mechanism for hydrazine synthesis: a three-electron reduction of nitric oxide to hydroxylamine at the active site of the γ-subunit and its subsequent condensation with ammonia, yielding hydrazine in the active centre of the α-subunit. Our results provide the first, to our knowledge, detailed structural insight into the mechanism of biological hydrazine synthesis, which is of major significance for our understanding of the conversion of nitrogenous compounds in nature.
Dinitrogen gas (N2) is a tough nut to crack. The atoms pair up with a triple bond, very difficult for humans to break without a lot of heat and pressure. Fortunately, this makes it very inert for the atmosphere, but life needs to get at it to make amino acids, muscles, organs, and more. Nitrogenase enzymes in some microbes, such as soil bacteria, are able break apart the atoms at ambient temperatures (a secret agricultural chemists would love to learn). They then "fix" nitrogen into compounds such as ammonia (NH3) that can be utilized by plants and the animals that eat them. To have a nitrogen cycle, though, something has to return the N2 gas back to the atmosphere. That's the job of anammox bacteria.
Most nitrogen on earth occurs as gaseous N2 (nitrogen oxidation number 0). To make nitrogen available for biochemical reactions, the inert N2 has to be converted to ammonia (oxidation number −III), which can then be assimilated to produce organic nitrogen compounds, or be oxidized to nitrite (oxidation number +III) or nitrate (+V). The reduction of nitrite in turn results in the regeneration of N2, thus closing the biological nitrogen cycle.
Let's take a look at the enzyme that does this, the "hydrazine synthase multiprotein complex." Rocket fuel; imagine! No wonder the scientific community was surprised. The formula for hydrazine is N2H4. It's commonly used to power thrusters on spacecraft, such as the Cassini Saturn orbiter and the New Horizons probe that went by Pluto recently. Obviously, the anammox bacteria must handle this highly reactive compound with great care. Here's their overview of the reaction sequence. Notice how the bacterium gets some added benefit from its chemistry lab:
Our current understanding of the anammox reaction (equation (1)) is based on genomic, physiological and biochemical studies on the anammox bacterium K. stuttgartiensis. First, nitrite is reduced to nitric oxide (NO, equation (2)), which is then condensed with ammonium-derived ammonia (NH3) to yield hydrazine (N2H4, equation (3)). Hydrazine itself is a highly unusual metabolic intermediate, as it is extremely reactive and therefore toxic, and has a very low redox potential (E0′ = −750 mV). In the final step in the anammox process, it is oxidized to N2, yielding four electrons (equation (4)) that replenish those needed for nitrite reduction and hydrazine synthesis and are used to establish a proton-motive force across the membrane of the anammox organelle, the anammoxosome, driving ATP synthesis.
We've discussed ATP synthase before. It's that rotary engine in all life that runs on proton motive force. Here, we see that some of the protons needed for ATP synthesis come from the hydrazine reaction machine. Cool!
What does the anammox enzyme look like? They say it has tunnels between the active sites. The "hydrazine synthase" module is "biochemically unique." Don't look for a common ancestor, in other words. It's part of a "tightly coupled multicomponent system" they determined when they lysed a cell and watched its reactivity plummet. Sounds like an irreducibly complex system.
The paper's diagrams of hydrazine synthase (HZS) show multiple protein domains joined in a "crescent-shaped dimer of heterotrimers" labeled alpha, beta, and gamma, constituted in pairs. The machine also contains multiple haem units (like those in hemoglobin, but unique) and "one zinc ion, as well as several calcium ions." Good thing those atoms are available in Earth's crust.
Part of the machine looks like a six-bladed propeller. Another part has seven blades. How does it work? Everything is coordinated to carefully transfer electrons around. This means that charge distributions are highly controlled for redox (reduction-oxidation) reactions (i.e., those that receive or donate electrons). The choice of adverbs shows that their eyes were lighting up at their first view of this amazing machine. Note how emotion seasons the jargon:
Intriguingly, our crystal structure revealed a tunnel connecting the haem αI and γI sites (Fig. 3a). This tunnel branches off towards the surface of the protein approximately halfway between the haem sites, making them accessible to substrates from the solvent. Indeed, binding studies show that haem αI is accessible to xenon (Extended Data Fig. 4c). Interestingly, in-between the α- and γ-subunits, the tunnel is approached by a 15-amino-acid-long loop of the β-subunit (β245-260), placing the conserved βGlu253, which binds a magnesium ion, into the tunnel.
We would need to make another animation to show the machine in action, but here's a brief description of how it works. The two active sites, connected by a tunnel, appear to work in sequence. HZS gets electrons from cytochrome c, a well-known enzyme. The electrons enter the machine through one of the haem units, where a specifically-placed gamma unit adds protons. A "cluster of buried polar residues" transfers protons to the active center of the gamma subunit. A molecule named hydroxylamine (H3NO) diffuses into the active site, assisted by the beta subunit. It binds to another haem, which carefully positions it so that it is "bound in a tight, very hydrophobic pocket, so that there is little electrostatic shielding of the partial positive charge on the nitrogen." Ammonia then comes in to do a "nucleophilic attack" on the nitrogen of the molecule, yielding hydrazine. The hydrazine is then in position to escape via the tunnel branch leading to the surface. Once they determined this sequence, a light went on:
Interestingly, the proposed scheme is analogous to the Raschig process used in industrial hydrazine synthesis. There, ammonia is oxidized to chloramine (NH2Cl, nitrogen oxidation number −I, like in hydroxylamine), which then undergoes comproportionation with another molecule of ammonia to yield hydrazine.
(But that, we all know, is done by intelligent design.)
So here's something you can meditate on when you take in another breath. The nitrogen gas that comes into your lungs is a byproduct of an exquisitely designed, precision nanomachine that knows a lot about organic redox chemistry and safe handling of rocket fuel. This little machine, which also knows how to recycle and reuse all its parts in a sustainable "green" way, keeps the nitrogen in balance for the whole planet. Intriguing. Interesting. As Mr. Spock might say, fascinating.
Saturday 17 June 2017
Why the quest to reduce biology to chemistry is doomed.
The White Space in Evolutionary Thinking
Ann Gauger
When certain biologists discuss the early stages of life there is a tendency to think too vaguely. They see a biological wonder before them and they tell a story about how it might have come to be. They may even draw a picture to explain what they mean. Indeed, the story seems plausible enough, until you zoom in to look at the details. I don't mean to demean the intelligence of these biologists. It's just that it appears they haven't considered things as completely as they should. Like a cartoon drawing, the basic idea is portrayed, but there is nothing but blank space where the profound detail of biological processes should be.
Let me give an example. This week Discovery Institute released a pair of videos ("How to Build a Worm" and "Switched on Worms") featuring Fellow and philosopher of biology Paul Nelson and a lowly nematode called C. elegans. Its development is precise and intricately patterned, like a Bach fugue that splits and weaves many voices into one. The final cadence is the newly hatched larva. Not coincidentally, the videos use music by Bach throughout.
Old CW chance and necessity did it/New CW gremlins did it
Evolution: The Fossils Speak, but Hardly with One Voice
Denyse O'Leary
Editor's note: We are delighted to inaugurate a new series, "Talk to the Fossils," by our friend and colleague Denyse O'Leary. See here for her Introduction.
University of Chicago biochemist James Shapiro, not a design theorist,offers in one of his lectures four kinds of rapid, evolutionary change that Darwin "could not have imagined": horizontal DNA transfer, symbiogenesis, genome doubling, and built-in mechanisms of genome restructuring. His approach is in sharp contrast to the "defend Darwin" strategy usually championed in the academy. So it is no surprise that he is a controversial figure. But is he right in saying that many possible mechanisms of evolution owe little or nothing to Darwin's theory, the only concept of evolution most of us hear about?
It is reasonably estimated that there are 8.7 million species today (excluding bacteria), but that only about 14 percent have been identified -- and only 9 percent of ocean life forms. Our picture of Earth's life forms might change radically if we had more information about all the others. For example, an entire kingdom of life, the Archaea, was only identified in the 1970s.
How did all these life forms get to be where they are? As we examine some evidence-based mechanisms, we should keep in mind a critical question: How does a given mechanism fit our current picture of evolution? And how much change can it account for?
The welter of data coming back from paleontology, genome mapping, and other studies presents a challenging picture. With so much new information, the history of life begins increasingly to resemble the history of human civilizations. There is peril in that, principally to older ideas that depended on less information and more overarching theory.
Overarching theories often falter when evidence replaces speculation. Darwinian evolution is, despite legislative protection, certainly one of the victims. By contrast, discarded and ridiculed theories like Lamarck's (inheritance of characteristics acquired in life by the parents) may turn out to have some basis in epigenetics.
So, to start this series, instead of contemplating yet another picture derived from grand theories, let us assemble, under eight headings, some of what we have learned in past decades that we did not expect. That might help us evaluate theories, new and old.
1. First, how reliable is the fossil record? It's really a question of what we don't know that would make a difference. Some sense of the difficulty may be gleaned from a comment offered by University of Bristol's Michael Benton:
Paleontologists are right to be cautious about the quality of the fossil record, but perhaps some have been too cautious. The sequence of fossils in the rocks more or less tells us the story of the history of life, and we have sensible ways of dealing with uncertainty. Some recent work on "correcting" the fossil record by using formation counts may produce nonsense results.
But which results are nonsense? How will we know?
2. Are there patterns in evolution? Yes, probably, at least two: Larger size and growing complexity (partly a function of multicellular body plans). Over the last 542 million years, marine animals' mean size has increased by 150 times. As it happens, the largest animal that has ever lived, so far as we know, is today's blue whale.
That said, patterns we assume to exist may not hold up. A classic evolutionary doctrine, "Dollo's law," claims that traits once lost can never be regained. But bone worms, for one example, seem to break this law, in that the males are roughly the same size as the females, instead of being the usual thousands of times smaller for their type of worm. Frogs, snapdragons, and snakes, among other life forms, apparently also break the law with impunity. From The Smithsonian, we learn that evolution is indeed reversible:
Some mites have returned to their free-roaming ways after countless millennia living on animal hosts. And a tree frog from South America lost its lower teeth only to re-evolve them after 200 million years.
We don't actually know how rare reversal is. And we can't fill in large chunks of time with patterns when there are no verified patterns. Some say Dollo's law is due for retirement. But others aver, using computer models, that evolution is both irreversible and unpredictable. If evolution is indeed unpredictable, there is no pattern.
Some, like science writer Philip Ball, claim nonetheless that there is a "strange inevitability of evolution." At Nautilus, he reports:
"Darwin's theory surely is the most important intellectual achievement of his time, perhaps of all time," says evolutionary biologist Andreas Wagner of the University of Zurich. "But the biggest mystery about evolution eluded his theory. And he couldn't even get close to solving it.
But wait! If the biggest mystery in evolution eluded Darwin's theory, why his theory "the most important intellectual achievement of his time, perhaps of all time"? How are we supposed to get anywhere if we are expected to venerate such a non-explanatory grand theory?
In reality, patterns in life forms are often wrongly interpreted when Darwinism is used as a frame. For example, current evolutionary theory provides no clear basis for interpreting a relationship between longevity and fertility. Thus, some researchers claimed that women undergo menopause but chimpanzees do not, that "menopause is not a part of the life cycle of living apes but has been uniquely derived in the human lineage."
Darwinian explanations for that are, of course, on offer. For example, men triggered menopause (by preferring younger women). Or women's selfish genes cause them to forego future breeding in order to invest in the survival of their existing selfish genes (children), sometimes called the grandmother hypothesis. That thesis assumes, of course, that older women are an asset to a group. Sometimes they are, sometimes not.
Despite all such claims, chimpanzees do undergo menopause, as a carefully researched 2012 paper on captive chimpanzees notes. But she-chimps do not typically live long after menopause. A recent article in Naturesummarizes the fact that current evolution theory provides no basis for interpretation of the relationship between longevity and fertility in life forms.
3. Life forms sometimes survive in ways we did not imagine, let alone predict.Some bacteria eat electrons, demonstrating "the almost miraculous tenacity of life." If some life forms live on pure energy, one wonders, will we one day discover life forms that live on pure information? Don't count it out.
And some life forms defy classification: The ancient (chancelloriid) "balloon animal" from over 500 mya doesn't seem to fit in with anything living today. And in a Chinese fossil trove from 570 mya, it is hard to decide whether the fossils are animals or bacteria. To quote a researcher, "What isn't widely appreciated is that the Doushantuo rock formation contains billions of microfossils, many of which have no traits that are diagnostic of any living group and contain features that are not of biological origin."
Another mysterious giant fossil that "seems to defy all known groups of organisms" is 450 million years old. Similarly, a billion-year-old microorganism is not apparently a fungus, alga, parasite, plant, or animal, so classifiers just called it "protozoa" (first life). Not that we know it was the first life, as the name implies.
Even when life forms can be classified, they may still present conundrums rather than gaps filled. For example, when a 60-million-year-old shrew-like mammal fossil turned up, a researcher noted, "The new dryolestoid, Cronopio, is without a doubt one of the most unusual mammals that I have seen, extinct or living."
Might there be life forms out there that are permanently unclassifiable using our present system? Maybe using a genetic code we don't understand? FromMotherboard, we learn, "There's already some evidence that something weird and undiscovered exists out there. Highly novel (and large) viruses, with weird strings of DNA (for a virus) have been discovered that seem to have strings of DNA from seemingly archaeal and eukaryotic genomes." If we take the ID approach seriously -- that DNA is a language -- the DNA might use different elements to form the instructional words, as long as they are functional in a given context.
Even when we can classify life forms, we are always finding forms that don't fit. Consider a recently discovered vegetarian relative of T. rex, an "evolutionary muddle of a beast," the size of a small horse, whose numbers dominated Patagonia 145 million years ago." We are promised "plenty of headaches for paleontologists hoping to place the animal in the dinosaur family tree." Also dubbed the platypus dinosaur, it mainly demonstrates that evolution studies don't feature much predictive power.
One could say the same of a huge, recently discovered North American dinosaur that could terrorize early tyrannosaurs 100 mya. "Contemporary tyrannosaurs would have been no more than a nuisance to Siats, like jackals at a lion kill."
So a whole narrative of late Cretaceous ecology got started entirely in ignorance of this top predator? That is like trying to understand the northern wilderness without knowing about the existence of bears. Or wolf packs. Similarly, the DNA of some ocean bacteria crucial to ecosystem healthdefies explanation, and "contradicts nearly all accounts of free-living microbial genome architectures to date."
Even when life forms do fit our beliefs, they don't always do what we say they must: A theory of animal origin, that complex life evolved because atmospheric oxygen levels began to rise about 630-635 million years ago, was challenged recently by the discovery that some early animals, including common sea sponges, need almost no oxygen.
Other life forms do things we assumed they could not: A living wasp has an ovipositor partially metal-plated with zinc. Why? "It must be hard but flexible so that the female wasp can curve and bore it through the fig. And the wasp must be able to use it repeatedly and efficiently without it wearing down or fracturing."
4. Beyond this, we keep discovering new life forms that we did not expect or predict. A newly discovered Pacific Northwest spider, announced in 2012, represents a hitherto unknown family, according to conventional classification, not just a new genus or species. Recently discovered mushroom-shaped sea creatures turn out to be neither jellyfish nor comb jelly, and could be related to groups thought to be extinct for over half a billion years. Or possibly a newly discovered branch on the tree of life.
We also keep finding new life forms that change the picture. A mystery mammal's tracks, found alongside those of dinosaurs, belong to a raccoon-size animal at a time (118 mya) when most mammals are thought to have been no bigger than a rat. Similarly, a new fossil find from 130 mya in Chinafeatures "not a parade of galumphing giants, but an assemblage of quirky little creatures like feathered dinosaurs, pterosaurs with advanced heads on primitive bodies, and the Mesozoic equivalent of a flying squirrel."
Yet despite all this, so far as our research can tell, non-life never exploits any strategy to become life. So one thing is still true: Pasteur's dictum, "Omne vivum ex vivo" ("All life comes [only] from life").
5. Far too much attention may be given to genes and DNA. So much current evolution thinking, including questionable fields like evolutionary psychology, depends on the alleged power of the gene. Does anyone remember that fellow who said in the early 90s that a CD of your genome is "you"?
Not even close. From the New Statesman: "According to a growing number of researchers, the standard story of the influence of genes is overblown. So many other factors influence how we turn out as individuals and how we evolve as a species that the fundamentals of biology need a rewrite." "This is no storm in an academic tearoom," a group of biologists wrote in the journalNature recently: "It is a struggle for the very soul of the discipline."
The gene isn't even necessarily what we think. Diverse genomes can exist in a single person: Mothers' cells may remain in their children and children's cells in their mothers decades after childbirth. So that CD of your genome is both you and your mom?
There are some relatively new genes. There are also "hidden" genes that don't show in current populations but might later. Some genes are not "junk" but also not strictly necessary either: "In the late 1990s a team of researchers at Stanford University created around 6,000 mutants of brewer's yeast, each of them lacking a different single gene, and found that many of them thrived just as well as the unmutated yeast did." No surprise there; successful life forms would feature redundant systems.
Some life forms can edit their genes extensively. Squid can, apparently. A researcher noted, "It was astonishing to find that 60 percent of the squid RNA transcripts were edited." The iconic fruit fly is thought to edit only 3 percent of its makeup.
Some species can have more than one genetic origin. Polyploidy, which means that the species has two complete sets of chromosomes, has been identified in a mimulus plant in Scotland. We learn that polyploids "are common among plants, as well as among certain groups of fish and amphibians. For instance, some salamanders, frogs, and leeches are polyploids." and "Mimulus peregrinus is an example of how some branches can come back together again and spawn new species that are in part the combination of their ancestors."
Basic claims about inheritance principles are also coming under fire. Researchers recently found that Mendel's "law of segregation" (an equal probability of inheriting each of two copies of each gene from both parents)doesn't always hold. We now learn, "For years, scientists had evidence that this law was being broken in mammals, but they didn't know how." Apparently, female mice pass on one copy of the R2d2 gene more frequently than the other copy. This finding, if it holds, matters because the probability of heritable illness is calculated by doctors assuming Mendel's Law. But maybe it's not a law.
Not surprisingly, some respected researchers now question the amount of attention given to the gene as such. A recent Royal Society paper denotes genes as "merely a means of specifying polypeptides." Whether the researchers are right or wrong, they add to a growing chorus against the vision of evolution that started with Darwin and was revived by Mendelian genetics, as natural selection acting on random mutation of genes to create the world of life we see around us.
6. Some data that garner attention in the pop science media sound counterfactual. For example, we are told by some researchers that evolution favors the collapse of cooperation, according to game theory:
"It's a somewhat depressing evolutionary outcome, but it makes intuitive sense," said [Joshua] Plotkin, a professor in Penn's Department of Biology in the School of Arts & Sciences, who coauthored the study with [Alexander] Stewart, a postdoctoral researcher in his lab. "We had a nice picture of how evolution can promote cooperation even amongst self-interested agents and indeed it sometimes can, but, when we allow mutations that change the nature of the game, there is a runaway evolutionary process, and suddenly defection becomes the more robust outcome."
Does it make intuitive sense? How is it that many of the most durable species are adept at co-operation, whether we are talking about humans, bees, or Canada geese? And do we know that a high-observed level of co-operation existed back in the Cambrian?
7. Some claims sound either trivial or politically sourced. For example, we are told, "Some species are evolving far more quickly than Darwin ever imagined." How? "Mosquitoes that colonized the London Underground in 1863 are now so different they can no longer mate with their above-ground relatives. Chinook salmon from Alaska to California needed just a human generation to become smaller and shorter-lived after an increase in commercial fishing in the 1920s. Adaptation is happening right under our noses, in our lifetimes." But all of this can be accounted for, assuming mere loss of information. It is gain in information that matters in evolution.
Then there is the assertion that human-caused climate change will spur the evolution of new species in an evolutionary surge, and that new species are beginning to emerge already. At last! A claim we can verify. What and where are these species?
More problematic are widely publicized false claims about "throwbacks" to earlier human evolutionary time. Some readers may recall the Turkish family that walks on all fours, as a supposed instance of "backward evolution" (along with human tails that turn out to be Photoshopped). But, contradicting earlier claims, a careful study showed that the family members do not walk in a diagonal pattern like apes or monkeys. They walk on all fours as other humans would, if asked to do so (laterally). Their unusual mobility is a response to an untreated human disorder, Uner Tan Syndrome (UTS). Many distressing conditions only come to attention when a person seeks modern medical diagnosis. Urban legends about "evolution" are an unwelcome distraction in such a case.
8. Evolution is often spoken of as if it were a deliberating intelligence, though the idea is considered a heresy. "Evolution," we are told by one respected source, has been "experimenting" with different types of early humans, based on the fact that skeletons show more diverse features than expected. That prompts two questions: If all the passengers in a subway car in a large, multicultural city met a mishap and were fossilized, how many "different species" would be identified today, using current methods? Second, is evolution (Evolution?) an intelligent agent? If it is not possible to speak of evolution's course without resort to the language of agency, is that a defect in human intelligence or an apprehension of fact?
Recently, the Washington Post ran a story about ten fossils that explain life on Earth. They only "explain" life on Earth if you think that ten disconnected headlines constitute an explanation.
Along those lines, we are now told at PBS that we must try thinking harder so that we will come to "believe in" evolution. But what specifically ought we to believe in? And is that really a way to approach science?
Instead, let us take a whirlwind tour of ways evolution is known to occur, as opposed to how grand theories say it occurs, and see what we can find out.
Image: La Brea Tar Pits, Los Angeles, by Charles Robert Knight [Public domain],via Wikimedia Commons.
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