Information 'R' us?

To Protect Genetic Information, Cells Go to Extraordinary Lengths

Evolution News & Views March 10, 2016 3:43 AM |

If the real "stuff" of the universe is information, as William Dembski argues in his book Being as Communion, it makes sense that life would make it a high priority to preserve that information. To a Darwinian who deals in chance processes, though, information is just a haphazard by-product of variation and selection. Some recent papers provide an opportunity to compare the explanatory success of both positions.

That DNA bears coded information has been non-controversial since the 1950s, of course, but we should not forget how revolutionary a concept that was. Before that, heredity reduced to chemistry. Some envisioned a homunculus in the cell, a reduced form of the organism that merely grew to maturity. Mendel conceived of alleles in pairs that accounted for traits. But to find that the carrier of heredity was a digital code inscribed on molecules must surely count as one of the most revolutionary findings in the history of science. It also made sense: the vast diversity of living things could be explained by complex specified information encoded in a universal chemical language.

Now we are in the throes of another revolution. Epigenetics is revealing codes above codes; systems of data flow, quality control, and information processing that cannot be reduced to DNA itself. Let's look at a few of these with an "information" focus.

The Local Stiffs

To be transcribed, DNA has to be accessible. If the double helix is too rigid or too loose, its readability is compromised. The double helix of DNA wraps around chromatin to form nucleosomes. This would seem to lock it away from the transcription machinery, but a remarkable set of molecular tags is coming to light that modulates the stiffness of the DNA strand on chromatin, so that it can "loosen up" when needed for translation, but stay rigid enough to be durable at other times.

These tags, called methyl groups (5-mC), formyl groups (5-fC) and carboxyl groups (5-caC), attach to cytosine bases in the DNA at the fifth carbon. The type of tag affects the flexibility of the strand, probably because of each tag's unique electrostatic signature. How this works was reported recently in Nature Communications by American biochemists at Eastern and Midwestern universities.

Molecular dynamics simulations show that these modifications promote or dampen structural fluctuations, likely through competing effects of base polarity and steric hindrance, without changing the average structure. The increase in DNA flexibility increases the mechanical stability of the nucleosome and vice versa, suggesting a gene regulation mechanism where cytosine modifications change the accessibility of nucleosomal DNA through their effects on DNA flexibility. [Emphasis added.]

The authors list the following possible functions for these tags:

5-mC is found in most plants, animals and fungi, and has aprofound effect on genome stability, gene expression and development. 5-hmC, 5-fC and 5-caC may also function in gene regulation. For instance, 5-hmC is preferentially enriched at distal regulatory elements such as enhancers in mouse or human embryonic stem cells, whereas 5-fC or 5-caC tend to accumulate at poised enhancers and promoters.Possible mechanisms for the regulatory role of cytosine modifications include the following: (1) altering the physical properties of DNA; (2) modulation of chromatin accessibility; and (3) recruitment of proteins that recognize cytosine modifications as their substrates followed by transcriptional activators/repressors that translate the presence of modifications to downstream signalling of transcription machinery.

If the proteins are recognizing these cytosine modifications, they are in essence reading a code that is independent of the DNA sequence. It's like calling out, "Tag found here; call in the activator." The activator signals the transcription machinery accordingly. That's fascinating enough, but the tag actually modifies the physical properties of DNA as well:

Here we report a comprehensive survey of the effect of cytosine modifications on DNA flexibility using a single-molecule cyclization assay: 5-fC remarkably increases DNA flexibility while 5-mC reduces and 5-hmC enhances flexibility, and 5-caC does not have a measurable effect. Molecular dynamics simulations elucidate the microscopic mechanism of the DNA flexibility changes induced by cytosine modifications.

They go on to describe in detail how this works (interested readers can study this open-access paper). Depending on the tags, they stiffen the strand to lift it from the chromatin, making it accessible to transcription machinery, or loosen the strand to allow it to wrap more tightly around the nucleosome. For example, "Methylation-induced increases in DNA stiffness likely arise from the restriction of the conformational fluctuations caused by the bulky methyl groups," possibly inactivating a gene. The 5-fc tag, by contrast, loosens the strand so that repair enzymes can get to repair a spelling error. These tags are not necessarily independent. The authors think they work together in a combinatorial way, modulating each other's influence. In addition, they appear numerically significant: the more 5-fc, the more stable the strand:

The presence of two copies of 5-fC in 147 bp (that is, 0.68%) of DNA of the 601 sequence results in a remarkable enhancement of nucleosome mechanical stability. This observation together with the reduced mechanical stability of nucleosomes containing many copies of 5-mC gives further support to our previously reported correlation between DNA flexibility and nucleosome stability: the more flexible DNA is, the more stably it is bound to histone octamer core and vice versa. The increased nucleosome stability induced by 5-fC may explain enrichment of 5-fC at poised enhancers and thetranscription start sites (TSSs) of low-expression genes:enhancement of nucleosome stability limits exposure of nucleosomal DNA to transcription machinery at enhancers and transcription start sites.

It's a work in progress that warrants further attention. But we're not done yet.

Tag Positional Roles

A commentary in Nature about a recent paper explores the impact of a methyl tag's position. Transcriptional regulation appears to be influenced not just by the presence of a methyl tag (CH3), but also by which nitrogen atom in an RNA base it is attached to. One such form, called m1A, was thought to be a bug; now it appears to be a feature.

Dominissini and colleagues' findings represent an intriguing step for epitranscriptomics. More work is needed tounderstand the mechanism by which m1A influences translation initiation and regulation, as well as the changes in its levels in stress responses. It will be exciting to see how this modification affects, and is affected by, RNA structure. Moreover, we need to know about the hypothesized proteins that are 'writers', 'readers' and 'erasers' of m1A and thus take part in the dynamics of its regulation. Finally, as yet another modified base has been identified in mRNAs, one wondershow many more exist: is this the final one, or are we just seeing the tip of the epitranscriptome iceberg?

Definitely exciting! Searching for "hypothesized writers, readers, and erasers" of these tags makes sense in light of the design perspective. They must be doing something important. But then, what is telling themwhat to do?

Signal to Noise

A paper in Current Biology explains how cells keep their focus on the signal in a noisy environment:

Transcriptional regulation is noisy, yet despite this variability,embryonic development reproducibly generates form and function. Recent work demonstrates that patterns of transcriptional activity in embryos are stably inherited through mitosis. These observations have implications for how accuracy arises in development.

What do the words "signal" and "accuracy" imply? Information, of course. This recalls our exploration of targets as a measure of intelligent design. It also makes one think of the chicken embryo sequence in Flight: The Genius of Birds that leads to a working chick at the end of a "highly elaborate dance" of many protein parts. The author of this paper puzzles over how the embryo gets to the target. One thing is certain: it works. The chick grows up to lay eggs that will grow more chickens that will lay eggs, maintaining the accuracy of the embedded coded instructions over thousands of generations.

Running the Replication Gauntlet

Think about the problem of maintaining genomic integrity during cell division. Machines are reading and duplicating DNA extremely rapidlywhile the cell is transcribing genes. This presents many challenges, not the least of which is avoiding extra copies of gene products. The number of proteins generated has to be tightly controlled, but now the cell has two DNA strands exposed to the transcription machinery, increasing in a stepwise manner. How does the cell keep the "DNA dosage" constant during this dynamic whirlwind of activity? How does the cell maintain "expression homeostasis"?

Now there's a challenge many of us never thought about. Three Israeli scientists explore possible answers in Science Magazine:

Genome replication introduces a stepwise increase in the DNA template available for transcription. Genes replicated early in S phase experience this increase before late-replicating genes, raising the question of how expression levels are affected by DNA replication. We show that in budding yeast, messenger RNA (mRNA) synthesis rate isbuffered against changes in gene dosage during S phase. This expression homeostasis depends on acetylation of H3 on its internal K56 site by Rtt109/Asf1. Deleting these factors, mutating H3K56 or up-regulating its deacetylation, increases gene expression in S phase in proportion to gene replication timing. Therefore, H3K56 acetylation on newly deposited histones reduces transcription efficiency from replicated DNA, complementing its role in guarding genome stability.Our study provides molecular insight into the mechanism maintaining expression homeostasis during DNA replication.

Information, Information, Information

There's a lot more one could say. PhysOrg talks about how certain proofreading enzymes physically "yank" on RNA to keep the splicing machinery from starting at the wrong spot. News from Nencki Institutein Poland explores why it is that one base substitution in non-coding DNAcan lead to disease (that's like having one spectator leave a stadium and affect the outcome of the game). A research site in Belgium adds an additional layer of complexity to the human protein landscape, revealing that shortened versions of proteins are not only conserved, but are tightly regulated and have functions. And Science tries to come up with a unifying model of epigenetic regulation, seeking to get a handle on the "intricate 'web' of proteins, chemical modifications, and RNA that together organize genomic DNA into chromatin."

Everywhere in life, it's information, information, information. Machines are reading, writing, and erasing signals, regulating transcription and translation, and ensuring the correct information gets the organism to the target. Information is duplicated, proofread, and buffered against changes. Information at one level regulates information at another level. It's hard to keep up with what science is learning about biological information.

If early geneticists could barely conceive of digital codes as the basis of life, early 1950s biologists hardly knew what the next sixty years would reveal about additional levels of information that regulate the newly discovered genetic code. Intelligent design theory is well positioned to lead the charge into biology's information age.

How the evo-devo revolution undermines Darwinism.

The Evo-Devo Revolution: LEGOs or Transformers?

Michael Denton March 7, 2016 3:31 AM

Editor's note: In his new book Evolution: Still a Theory in Crisis, Michael Denton not only updates the argument from his groundbreaking Evolution: A Theory in Crisis (1985) but also presents a powerful new critique of Darwinian evolution. This article is one in a series in which Dr. Denton summarizes some of the most important points of the new book. For the full story, get your copy of Evolution: Still a Theory in Crisis. For a limited time, you'll enjoy a 30 percent discount at CreateSpace by using the discount codeQBDHMYJH.

he revolution associated with the field of evo-devo (evolutionary developmental biology) has brought with it the revelation that underlying the development of all organisms is a set of highly conserved gene circuits and integrated developmental modules that guide and constrain phylogeny without regard for the immediate adaptive needs of species. This new knowledge poses a widely acknowledged challenge (and indeed self-evident challenge) to Darwinian evolution.

And it has also undermined completely the previous neo-Darwinian mechanistic view of organisms as analogous to contingent assemblages of LEGO blocks. According to the Darwinian model, organisms are infinitely plastic "additive functional assemblages" which can be changed -- LEGO block by LEGO block -- from one shape to any other conceivable novel shape bit by bit without any significant constraints. On the contrary, all the evo-devo evidence suggests that there are deep and profound developmental constraints that work against such infinite pliability.

The new conception of organisms arising from the discoveries of evo-devo might be termed the "Transformer" model. Just as in a child's Transformer toy action figure, the number of forms that can be reached by combining the basic parts in different ways is severely limited by the shape and properties of the component building bricks. The finite set of forms that can be assembled is prefigured into the basic properties of the constructional units. One might view the constraints imposed by the building units in a Transformer set (unlike LEGO bricks) as being analogous to those imposed in living things by the highly conserved toolkit components and developmental modules.

Consequently, pigs will never fly -- not only because of functional constraints (far too heavy!), but because of deep internal structural constraints in the way a pig is put together, which greatly restrict the available paths that adaptive evolution can take. On this view, the major novelties actualized during evolution could only have occurred if they were compatible with the pre-existing inner "developmental logic" of the organism, analogous to prefiguring of the Transformer components for a specific set of forms.

In other words, development rules! Or, more precisely, what rules is the collective constraints of toolkit elements, developmental pathways, and modules that underlie the ontogeny of every class of metazoan organisms.

Although there are some dissenters,1 the existence of highly conserved developmental genetic mechanisms, gene circuits, and so forth restricting the paths of evolution has led to the widespread adoption of what might be termed a new constraints paradigm among many evo-devo researchers, who acknowledge that the deep logic of development is bound to restrict the direction of variation and hence evolutionary change along limited paths.2 But what is really radical about the "constraints paradigm" is that the constraints restrict the paths of evolution without any regard for immediate adaptive function."3

The notion of deeply shared non-adaptive internal causal factors channeling evolution in such a manner is certainly heretical. It is small wonder that, as Gerd Müller and Massimo Pigliucci concede, many leading biologists feel that evo-devo presents "challenges to the received theory... so substantial that no reconciliation with the classical framework [Darwinian, incremental functionalism] is at all possible."4

References:

(1) Hopi E. Hoekstra and Jerry A. Coyne, "The Locus of Evolution: Evo Devo and the Genetics of Adaptation," Evolution; International Journal of Organic Evolution 61, no. 5 (May, 2007): 995-1016; see also Lindsay R. Craig, "Defending Evo-Devo: A Response to Hoekstra and Coyne,"Philosophy of Science 76, no. 3 (2009): 335-344.

(2) Wallace Arthur, Evolution: A Developmental Approach; Jerry Fodor and Massimo Piattelli-Palmarini, What Darwin Got Wrong (London: Profile, 2010), Chapters 2, 3, and 4; Günter P. Wagner, Homology, Genes, and Evolutionary Innovation (Princeton: Princeton University Press, 2014).

(3) Ron Amundson, The Changing Role of the Embryo in Evolutionary Thought (Cambridge: Cambridge University Press, 2007), 8.

(4) Gerd B. Müller and Massimo Pigliucci, "Extended Synthesis: Theory Expansion or Alternative?" Biological Theory 5, no. 4 (2010): 275-276, 275.

Darwinism vs the real world XXIII

Diabetes: When Blood Glucose Control Fails

Howard Glicksman March 9, 2016 2:06 PM

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." For the complete series, see here. Dr. Glicksman practices palliative medicine for a hospice organization.

In my last article, we saw that the body uses glucose for its energy needs and after a meal, stores it within the liver and other organs in the form of glycogen and fat. Since the brain cannot store glucose, it is totally dependent on the liver's ability to release this stored energy several hours after a meal.

Real numbers have real consequences and if the blood glucose drops below 50 units, symptoms of brain malfunction, like weakness, dizziness, and problems with concentration occur. If it drops below 40 units, then problems with speaking and increased confusion and drowsiness occur. If it goes below 30 units, seizures and coma result. And when the blood glucose drops under 20 units, brain death is certain. Being able to control the blood glucose is critical for human survival and it doesn't just happen because we eat and drink sugary things. It requires the body to know when to store glucose and when to release it so the brain is always receiving what it needs.

The body uses what biochemist Michael Behe would call an irreducibly complex system, involving beta and alpha cells in the pancreas that controls its blood glucose. After a meal, the beta cells, using glucosensors, react to a rise in blood glucose above 70 units by releasing insulin. Insulin travels in the blood and attaches to specific receptors on target cells, particularly in the liver, telling them to take in glucose and store it as glycogen and fat. In contrast, several hours after a meal, the alpha cells, also using glucosensors, react to a drop in blood glucose below 70 units by releasing glucagon, which travels in the blood and attaches to specific receptors on target cells, mainly in the liver, telling them to release the glucose from glycogen and other energy storage molecules into the blood. It is important to note that due to their breakdown by enzymes, the metabolic effect of a given amount of insulin or glucagon only lasts a few minutes allowing for moment-to-moment blood glucose control within the body, along with the ratio of insulin and glucagon.

However, since the blood glucose must stay above a certain level for proper brain function, it is clear that just being irreducibly complex is not enough for a system to survive. It also has to have natural survival capacity.It must inherently know what the blood glucose level should be and give the conscious mind fair warning to do something if it begins to fall, like eating something. Having a low blood glucose level (hypoglycemia) can take place due to liver failure and rare tumors called insulinomas that send out too much insulin. However, the commonest cause for life-threatening hypoglycemia is when diabetics, who are prone to having too high of a blood glucose, accidentally take too much medication.

The serious consequences of a blood glucose level that is too low make sense, because the body needs glucose for energy. But why should too high of a blood glucose level be a problem? The laws of nature, those mysterious powers that evolutionary biologists claim to be responsible for our own existence, are responsible for the terrible consequences of high blood glucose. Why?

In the early winter of 1922 the parents of Leonard Thompson, a 14 year-old boy suffering from the incurable sugar disease, brought him to the University of Toronto, hoping he could receive an experimental treatment. For the several months prior, the previously healthy teenager had been urinating very frequently, was always thirsty, had lost a lot of weight, and was very weak. The doctors had said that he had diabetes mellitus, a condition that derives its name from the frequent passing of large amounts of sweet smelling urine due to high blood levels of glucose. Dr. Frederick Banting and his assistant, Charles Best, had isolated the pancreatic hormone they had initially named isletin (later changed to insulin) and had used it to successfully treat dogs with the same condition. Banting and Best knew that it was a deficiency of insulin that caused this disorder in glucose metabolism. Leonard Thompson was the first human to receive insulin and the resulting dramatic improvement in his condition gave hope to following generations of diabetics.

Diabetes mellitus is a chronic disorder where glucose metabolism is inhibited by inadequate insulin activity. Medical science has classified diabetics as being of one of two types.

Type I diabetics tend to be diagnosed earlier in life due to frequent urination, weakness, and weight loss because they have a deficient production of insulin and therefore very low amounts of insulin in the blood. Their blood glucose levels are usually extremely high, usually between 500 to 1,000 units at the time of diagnosis. Because they have very low levels of insulin, they must be started on injections of insulin right away.

Type II diabetics usually have a silent disease for many years; often it isn't diagnosed until they have a routine blood test or they suffer a complication (like a heart attack, recurrent skin infections, or numbness of the feet). Their symptoms are caused by normal or increased amounts of insulin, to which tissues, like the liver and muscles, do not respond well enough (insulin resistance). When diagnosed, most Type II diabetics are overweight. Insulin resistance and their blood glucose can improve with dietary restriction and weight loss, in addition to oral medical therapy, often foregoing the need for insulin injections.

Leonard Thompson was a Type I diabetic and, without adequate insulin activity, his body had problems with uptake, usage, and storage of glucose in the tissues. In addition, having inadequate insulin activity released his alpha cells from insulin suppression, thereby increasing the relative effects of glucagon in his body. The effect of having more than normal glucagon activity compared to insulin activity meant that his body tended not to store glucose, synthesize protein or make fat. Instead, under the influence of glucagon, his body constantly thought it needed to make glucose from the breakdown of protein and fat, and to convert free fatty acids into ketones to help energize his brain. In other words, without enough insulin, the body has difficulty informing the tissues that they are in the fed state and should be storing glucose. Since glucagon dominates the metabolism, the tissues think that the body is always in starvation mode despite having a high blood level of glucose.

Without having enough insulin to promote the efficient uptake of glucose in the liver, muscles, and fat cells, the amount of glucose absorbed from the digestive system results in very high levels of blood glucose. This is where the laws of nature take hold. High blood glucose causes high glucose in the fluid filtered within the kidney tubules, overwhelming its ability to reabsorb it. This causes the body to lose glucose and calories. Additionally, the high glucose content of the filtered fluid in kidneys causes an osmotic diuresis. Because the total chemical content in the filtered fluid is so high, by the power of osmosis, the kidneys must give up too much water, losing the ability to maximally concentrate the urine, causing excessive water loss.

In addition, the high blood glucose level also makes water naturally move out of the cells through osmosis. The combination of too much water leaving the cells and the kidneys, and losing too much water, all due to osmosis, ultimately results in profound dehydration, often leading very low blood pressure. Finally, since the body thinks it is in starvation mode and doesn't have enough glucose, it starts forming alternative chemicals for energy use for the brain by producing more ketones, which are acids. The build-up of these ketones causes a rise in the H+ion level resulting in acidosis, which is toxic to cells and ultimately leads to death.

It was this one-two punch of severe dehydration and acidosis that alterted Leonard Thompson's doctors to the fact that he didn't have long to live. Receiving the insulin injections from Banting and Best helped correct his body's ratio of insulin and glucagon and allowed him to live another thirteen years, dying of pneumonia at the age of 27. It is important to note, however, that although a person can live for only a few months without insulin, the absence of glucagon is incompatible with life.

The laws of nature determine what blood glucose level is necessary for the body to survive. Since the body, the brain in particular, requires a certain amount of energy to function properly, there must be sufficient glucose in the blood at all times. In addition, because of osmosis, if the blood glucose rises too high, this can lead to severe dehydration. Finally, because the lack of insulin makes the body produce other sources of energy that the brain can use (ketones) it causes the H+ ion level in the blood to increase to toxic levels which can cause death from diabetic ketoacidosis.

When it comes to controlling the blood glucose, these are the three ways the laws of nature affect human life. Without the irreducibly complex system that uses glucosensors on pancreatic cells that produce insulin and glucagon, human life would be impossible. Evolutionary biologists expect us to believe that all of this developed by chance and the laws of nature alone. But life is still more complicated. When the body breaks down glucose in the presence of oxygen, most of the energy is released as heat. This means that the higher the metabolic rate, such as with increased activity, the more heat the body generates.

However, since the enzymes in the cells only work properly within an optimal temperature range, this means that with changes in metabolic activity, the body must make sure it keeps its core temperature within certain limits. How does the body maintain control and does it make sense that it came about by chance and the laws of nature alone? That's what we'll begin to explore next time.

Another failed Darwinian prediction XIII

Gene and host phylogenies are congruent

Evolution predicts that genetic change drives evolutionary change. Genetic changes that confer improved fitness are more likely to be selected and passed on. All of this means that evolutionary trees based on comparisons of genes should be similar, or congruent, with evolutionary trees based on comparisons of the entire species. Simply put, gene trees and species trees should be congruent. But while this has often been claimed to be a successful prediction, it is now known to be false. As one study explained, “Perhaps most unexpected of all is the substantial decoupling, now known in most, although not all, branches of organismal life, between the phylogenetic histories of individual gene families and what has generally been accepted to be the history of genomes and/or their cellular or organismal host lineages.” (Ragan, McInerney and Lake)   The molecular and the visible (morphological) features often indicate “strikingly different” evolutionary trees that cannot be explained as due to different methods being used. (Lockhart and Cameron) Making sense of these differences between the molecular and the morphological features has become a major task, (Gura) so common that it now has its own name: reconciliation. (Stolzer, et. al.)   The growing gap between molecular analyses and the fossil record, concluded one researcher, “is astounding.” (Feduccia) Instead of a single evolutionary tree emerging from the data, there is a wealth of competing evolutionary trees. (de Jong) And while the inconsistencies between molecular and fossil data were, if anything, expected to be worse with the more ancient, lower, parts of the evolutionary tree, the opposite pattern is observed. As one study explained, “discord between molecular divergence estimates and the fossil record is pervasive across clades and of consistently higher magnitude for younger clades.” (Ksepka, Ware and Lamm)   One interesting example is the Orangutans which share many similarities with humans. These “people of the forest,” as they have been called, have more in common with humans than do the other great apes. This includes features of anatomy, reproductive biology and behavior. But there is one feature in which orangutans are not the closest species to humans: the genome. The chimpanzee has the closest genome to the human genome, so it is thought to be our closest relative. The molecular and morphological comparisons point to incongruent phylogenies. As one paper concluded:   There remains, however, a paradoxical problem lurking within the wealth of DNA data: our morphology and physiology have very little, if anything, uniquely in common with chimpanzees to corroborate a unique common ancestor. Most of the characters we do share with chimpanzees also occur in other primates, and in sexual biology and reproduction we could hardly be more different. It would be an understatement to think of this as an evolutionary puzzle. (Grehan)   If it weren’t for DNA, it would be the orangutan rather than the chimp pictured next to the human in the evolutionary tree.   References   de Jong, W. 1998. “Molecules remodel the mammalian tree.”Trends in Ecology & Evolution, 13:270-275.   Feduccia, A. 2003. “‘Big bang’ for tertiary birds?.” Trends in Ecology & Evolution 18:175.   Gura, T. 2000. “Bones, molecules...or both?.” Nature 406:230-233.   Grehan J. 2006. “Mona Lisa smile: the morphological enigma of human and great ape evolution.” The Anatomical Record Part B: The New Anatomist 289B:139-157.   Ksepka, D. T., J. L. Ware, K. S. Lamm. 2014. “Flying rocks and flying clocks: disparity in fossil and molecular dates for birds.” Proceedings of the Royal Society B 281: 20140677.   Lockhart, P., S. Cameron. 2001 “Trees for bees.” Trends in Ecology and Evolution 16:84-88.   Ragan, M., J. McInerney, J. Lake. 2009. “The network of life: genome beginnings and evolution.” Philosophical Transactions of the Royal Society B 364:2169-2175. Stolzer, M., et. al. 2012. “Inferring duplications, losses, transfers and incomplete lineage sorting with nonbinary species trees.” Bioinformatics 28 ECCB:i409–i415.

On newly discovered Japanese plant species' surprising survival strategy.

New underground plant hides from the sun and parasitises fungi:

It’s a low-down, dirty cheat. A newly discovered Japanese plant spends most of its life hidden underground and steals nutrients from fungi rather than getting its energy from the sun.

Kenji Suetsugu of Kobe University came across the previously unknown plant in an evergreen forest on the subtropical Japanese island of Yakushima while documenting other fungi-parasitising – mycoheterotrophic – plants in Japan.

The plant’s stem is about 3-9 centimetres long and has between nine and 15 purple star-shaped flowers, which push up above the ground. Suetsugu has named it Sciaphila yakushimensis after the island.

The plant can’t photosynthesise and, like other mycoheterotrophs, steals the carbon it needs from a fungal host. The parasitic plant attracts strands of mycorrhizal fungus into its many hairy roots and then feeds off fungus growing inside the roots.

Life in the dark
Its parasitic lifestyle is an adaptation to the forest understorey, where the sun’s rays struggle to penetrate and so photosynthetic plants are rare, says Suetsugu.

Because it doesn’t rely on photosynthesising the sun’s light for its energy, it can stay underground, reducing the risk of being eaten by aboveground herbivores. It only pokes through the leaf litter to flower and fruit.

Vast fungal networks in the forest soil are linked up with plant roots and usually get their carbon from trees, in exchange for water and minerals that their tiny hairs extract from soil.

But mycoheterotrophs taps into this network and get the carbon from fungi, which got it from other plants to start with.

“These mycoheterotrophs are extremely rare and could not survive without a flourishing forest, sustained by species-rich underground fungal networks,” says Suetsugu.

Rare but not protected
Given that it only seems to have two small populations, the new species can be considered critically endangered, Suetsugu says. Other mycoheterotrophic plant species have recently been found in the area, but many are not yet officially protected.

Such plants are dependent on their host fungi, so Suetsugu says it will be necessary to conserve entire ecosystems to protect these rare plants. He recommends that regulators should restrict logging and construction to preserve these and other endemic species in the forest habitats of Yakushima.

Constantijn Mennes at the Naturalis Biodiversity Center in Leiden, the Netherlands, says there is still a substantial amount of undescribed biodiversity, even in flowering plants.

“This observation adds to a large list of critically endangered mycoheterotrophic species, like species of Kupea and Kihansia in Africa,” he says.


Journal reference: Journal of Japanese Botany, Vol. 91 No. 1

On theistic naturalism's false dichotomy

The False Dichotomy Between Intelligent Design and Natural Causes
Casey Luskin 

In a previous article in this series, we saw that a self-described theistic evolutionist had left the BioLogos camp because he was concerned about the way BioLogos writers treat Darwin-critics:
I have got used to the vituperative and often incoherent level of discussion about faith and evolution in the last year or so. Generally speaking, as one would now expect, Gnus attempting to savage anything they can identify as a theist are the greatest offenders. But on BioLogos, a frighteningly similar kind of abuse, if usually expressed with more gentility, is directed not back at non-theists, nor even YECs, but at ID sympathisers....I think I can draw two tentative conclusions about the reasons for this degree of passion, which is clearly far more than an opinion that ID arguments are wrong. In my opinion, although BioLogos is quite a diverse forum, its "ruling spirit" is fundamentally committed to (a) methodological naturalism and (b) theological naturalism.
How does the "theological naturalism" of BioLogos influence its perspective on intelligent design (ID)? Unfortunately, for one, it seems to lead some ID-critics to wrongly think that ID denies that God can use natural causes.

For example, in his series on "Evolution and the Origin of Biological Information," Dennis Venema sets up a false dichotomy between intelligent design (ID) and natural causes, wrongly claiming ID that creates a "'natural versus God' dichotomy" or alternatively claiming that ID tries to "eliminate the possibility of divine action" when "we use science to understand natural cause and effect." Venema also states:
[D]escribing how specified information can arise through natural means does not in any way imply God's absence from the process. After all, natural processes are equally a manifestation of God's activity as what one would call supernatural events. So-called "natural" laws are what Christians understand to be a description of the ongoing, regular and repeatable activity of God. As such, the dichotomy presented in ID writings of "naturalism" versus theism is a false one: is not God the Author of nature, after all?
While defending naturalism, Venema has badly misstated the claims of ID: there is no false dichotomy in intelligent design that says God is never allowed to use natural causes. The only party who's setting up a false dichotomy here is Dennis Venema, in suggesting that if one accepts ID then God is no longer allowed to use "natural laws." 

Venema seeks to paint ID as bad theology which somehow denies that God is the author of all nature when God uses secondary material or "natural" causes. ID is a scientific theory and doesn't make such theological claims. Thus, as a science, ID never claims that if we observe the "ongoing, regular and repeatable activity" of "natural laws" then somehow God is absent from the process.

ID proponents who believe in God never deny that God can use secondary material "natural" causes to achieve his will. In those instances, ID would simply say that material causes are the best explanation. ID does not "eliminate the possibility of divine action" when "we use science to understand natural cause and effect." To wit: ID proponents have often inferred design from the fine-tuning of the laws that govern the universe and make it friendly for life. Indeed, this is an area where BioLogos supposedly agrees with intelligent design. In any event, Venema's description of ID is backwards: in contexts of physics and cosmology, the actions of natural laws themselves can trigger a design inference.

Remember, ID is a cautious scientific theory and not a theological doctrine. When ID theorists look for scientifically detectable design at the biological level, they often treat natural causes as background. So the biological design that's detected normally involves features that (1) go well beyond the capacities of natural causes, and (2) exhibit telltale signs of intelligent agency (such as being the product of foresight). On the other hand, when ID infers a natural cause, pro-ID theists would simply say God used a natural cause, and would not say that God is somehow "absent."

All theists who support ID affirm that God is behind, in some sense, every event. "Natural cause" never means (for theists anyway) "not caused by God." I'm not aware of any ID theorist who is also a theist who has ever claimed otherwise.

This leads us to the question, why does ID critique theistic naturalism, and how does ID contrast with theistic evolution?

Theistic naturalism isn't merely the view that God at times (or even most of the time) works through natural causes. Rather, it is the view that assumes that God must only use natural causes and is never allowed to work in other ways that might break the "ongoing, regular and repeatable activity" of "natural laws." 

ID rejects such assumption-based views. ID is entirely compatible with the view that God at times (or even most of the time) works through natural causes. But ID isn't precommitted to answers about how God must have acted, and leaves open the possibility that sometimes God doesn't use "natural" causes. ID simply wants to follow the evidence where it leads. 

Thus, theistic naturalism is the wholesale assumption that if God exists, He must always use secondary material causes, and is never allowed to act in nature in a scientifically detectable way. The reason ID proponents critique naturalism is because it tends to presuppose materialistic answers to all questions about how life arose and diversified.

There are thus two potential extreme positions in this debate: (A) Everything is detectably designed and God never uses natural causes, or (B) Nothing is detectably designed and God always uses natural causes. 

Ironically, though ID critics (wrongly) accuse ID proponents of adopting extreme position (A), it is ID-critics themselves, including many theistic evolutionist proponents of theistic naturalism, who seem to adopt extreme position (B). This makes for bad science because it presupposes the scientific answers, and bad theology because it tries to dictate to God what He ought to do. 


In contrast, ID rejects both extreme positions, and uses this motto: let's not presuppose answers, but let's follow the evidence where it leads.

From the Cambrian era,further reason to doubt Darwin.

From the Cambrian Explosion, a Remarkably Preserved Image of a Nervous System
David Klinghoffer March 2, 2016 3:54 AM

Quite beautiful, isn't it? Like a dragon float from a Chinese New Year parade. The Washington Post calls it an "ugly arthropod." Are they blind?

News from Cambridge University of an unprecedented Cambrian find from, in fact, China:

A 520 million-year-old fossilised nervous system -- so well-preserved that individually fossilised nerves are visible -- is the most complete and best example yet found, and could help unravel how the nervous system evolved in early animals.

How did this arthropod's nervous system "evolve"? Suddenly, it seems, all but out of a clear blue sky, as far as we have any reason to say. What's striking about the new images of Chengjiangocaris kunmingensisis, a product of the Cambrian explosion, is the remarkable detail preserved from soft tissue. The difficulty of preserving soft tissue was once given as a reason that the Cambrian animals' precursors seem not appear in the fossil record.

At some earlier stage of life's history, these features were not there -- then they were. This is said to help "unravel" the mystery of evolution. More:

Researchers have found one of the oldest and most detailed fossils of the central nervous system yet identified, from a crustacean-like animal that lived more than 500 million years ago. The fossil, from southern China, has been so well preserved that individual nerves are visible, the first time this level of detail has been observed in a fossil of this age.

The findings, published in the Proceedings of the National Academy of Sciences, are helping researchers understand how the nervous system of arthropods -- creepy crawlies with jointed legs -- evolved. Finding any fossilised soft tissue is rare, but this particular find, by researchers in the UK, China and Germany, represents the most detailed example of a preserved nervous system yet discovered.

Again, the question of what this means for evolution:

For [Javier Ortega-Hernández, of the University of Cambridge's Department of Zoology,] and his colleagues, a key question is what this discovery tells us about the evolution of early animals, since the nervous system contains so much information. Further analysis revealed that some aspects of the nervous system in C. kunmingensis appear to be structured similar to that of modern priapulids (penis worms) and onychophorans (velvet worms), with regularly-spaced nerves coming out from the ventral nerve cord.

In contrast, these dozens of nerves have been lost independently in the tardigrades (water bears) and modern arthropods, suggesting that simplification played an important role in the evolution of the nervous system.


The nervous system is information rich, and "these dozens of nerves" were lost by tardigrades and today's arthropods. These latter creatures evolved in part by losing information, not gaining it -- becoming simpler, not more complex. So where did the information come from in the first place? They don't say. They can't say.

Darwinism vs. the real world XXXII

Absorbing and Storing Energy: How the Body Controls Glucose
Howard Glicksman March 2, 2016 4:44 PM 


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.


Just like a car needs the energy, in the form of gasoline, to run properly, the body needs the energy in glucose to survive. When we haven't eaten for a while, our blood glucose level drops and our stomach is empty, causing the hunger center in our brain to tell us to eat or drink something with calories. As I have explained in my last couple of articles, the complex molecules that are in what we eat and drink enter the gastrointestinal system, where digestive enzymes break them down into simpler molecules so the body can absorb them. Carbohydrates are broken down into simple sugars, like glucose, which are then absorbed into the blood. Tissues, such as the brain and other organs, rapidly absorb some of this glucose, to be used for their immediate energy needs.

However, the amount of glucose absorbed after a meal is usually much more than what the tissues can use right away, causing excess. The body is able to chemically link these excess glucose molecules together to form a carbohydrate called glycogen. Most of the glycogen in the body is made and stored in the liver, with smaller amounts in the muscles, kidneys, and other tissues. Once the liver and other tissues have filled up their glycogen stores, any excess glucose is stored as fat, apparently without limit. These tissues can use this stored energy in between meals, during exercise, and fasting overnight, when there aren't any new supplies of glucose coming into the body. However, the brain cannot store glucose and is mostly dependent on the glucose in the blood for all of its energy needs.

One way the body makes sure the brain receives enough glucose during fasting is to have the liver release glucose from its glycogen stores into circulation. The liver has the capacity to store enough glucose to meet all of the body's energy needs for about 24 hours. In addition, when necessary, the liver can take certain proteins and fats and convert them into glucose and other molecules, called ketones, that the brain can use for energy as well. This is partly why we don't have to eat food as often as we have to breathe or drink water. But clinical experience teaches that not just any blood level of glucose will do for human survival. Real numbers have real consequences and the brain always needs a certain amount of glucose. Even though the body may be physically at rest, the brain is always working hard. It must keep us awake, monitor what's going on inside and around us, and control vital functions like breathing and circulation.

Between meals, the blood glucose level usually runs between 70-90 units. Several hours after we eat, when the blood glucose level starts to drop towards 70 units, our hunger center warns us to eat something. If the blood glucose drops below 50 units, symptoms of brain malfunction, like weakness, dizziness, and problems with concentration occur. If it drops below 40 units, you'll probably start experiencing problems speaking, confusion, and drowsiness. Below 30 units, seizures and coma result, and below 20 units, brain death is certain. Being able to control the blood glucose is important for human survival and it doesn't just happen because we eat and drink things that have sugar in them. It requires the body to know when to store glucose and when to release it so the brain is always receiving what it needs. Here's how the body does it.

As we've seen in this series, the first thing you need to take control is a sensor that can detect what needs to be controlled. The pancreas is not only an exocrine gland that, as noted in the previous articles, sends fluid containing various chemicals and enzymes into the intestine to help digest food. It is also an endocrine gland that sends hormones into the blood to help control the blood glucose. Scattered throughout the pancreas are small clumps of cells that make up what is called the islets of Langerhanswhich perform this endocrine function. These cells have glucosensors,allowing them to detect the blood level of glucose.

The second thing you need to take control is something to integrate the data, decide what needs to be done, and then send out a message. There are two different types of gland cells in the islets of Langerhans that together control the blood glucose. One is the beta cell,which sends out a hormone called insulin,made up of 51 amino acids joined together in a specific order. After a meal, the more the blood glucose rises above 70 units (it normally peaks at about 110 units), the more insulin the beta cells release into the blood. However, several hours after eating, as the blood glucose drops toward 70 units and below, the beta cells reduce the levels of insulin they send out. The other cell is the alpha cell, which sends out a hormone called glucagon,made up of 29 amino acids joined together in a specific order. Several hours after a meal, when the blood glucose drops toward 70 units and below, the more glucagon the alpha cells send out and after a meal, the more the blood glucose rises above 70 units, the less glucagon the alpha cells send out.

As you can see, both the beta and alpha cells have glucosensors, but they respond to changes in blood glucose in opposite ways. Normally, the higher the blood glucose rises above 70 units, the more insulin the beta cells send out and the less glucagon the alpha cells send out. And when the blood glucose drops toward 70 units and below, the less insulin the beta cells send out and the more glucagon the alpha cells send out.

The third thing you need to take control is an effector that can do something about the situation. After a meal, the blood glucose rises because the amount of glucose brought into the blood is more than what the body can use right away. As noted above, the beta cells react to this rise in blood glucose by sending out more insulin. Insulin travels in the blood and locks onto specific receptors within target organs, especially the liver, and tells them to absorb glucose for energy and store what is left over. In general, insulin is an anabolic hormone, e.g. it promotes the formation of more complex molecules from simpler ones. Not only does insulin promote the formation of glycogen from glucose in the liver and muscles, it also tells some cells to take in amino acids to form proteins and others to take in fatty acids to form fats. In other words, insulin tells the body "We've just been fed and we've got more than we need right now. Store up the excess for later use."

In contrast, several hours after a meal, the blood glucose falls as the body takes glucose out of the blood and uses it for its energy needs without new supplies coming in through the gastrointestinal system. As I noted, the alpha cells react to this drop in blood glucose by sending out more glucagon. Glucagon travels in the blood where it locks onto specific receptors on target cells, mainly in the liver, and tells them to release the glucose from within glycogen and other forms of stored energy. In general, glucagon is a catabolic hormone, which promotes the breakdown of more complex molecules into simpler ones. Not only does glucagon cause glucose to be released from the glycogen stores, it also tells cells to break down certain proteins and fats into glucose and ketones, so the brain can be use them for energy. In other words, glucagon tells the body "We haven't been fed for a while. Release the energy we stored up before."

Once again, you can see that insulin and glucagon order the liver and other cells to do things that are opposed to each other. Insulin tells the body when it is fed and must take glucose out of the blood and store it in the liver and fat cells for later use. Glucagon tells the body when it is in starvation mode and must release glucose and other chemicals from the liver and fat cells into the blood so the brain will have enough energy. It is important to note that due to the breakdown by enzymes, the metabolic effect of a given amount of insulin or glucagon only lasts a few minutes and along with the ratio of insulin and glucagon this allows for moment-to-moment blood glucose control within the body.

There are twenty different amino acids that make up the proteins in the body. Since insulin consists of 51, and glucagon, 29 amino acids arranged in a specific order, this means that the chances of one molecule of each of them coming into being at random is one in 1066 for insulin and one in 1038 for glucagon. It was this extremely high improbability of any one of the thousands of biologically significant molecules, such as insulin and glucagon, being formed by chance and the laws of nature, which alerted scientists that the cells must have an intelligent agent telling them how to make them.

This is what first motivated scientists to search for and find the DNA molecule. However, paradoxically, evolutionary biologists see all of the information packed into the DNA molecule and still conclude that it all came about by chance and the laws of nature alone rather than through a mind at work. In other words, scientists, using their ability to detect intelligence, recognized that there had to be an intelligent agent inside the cell instructing it on how and when to produce these complex and vital molecules, but after finding it, concluded that this intelligent agent itself had come about by chance and the laws of nature alone.

Alternatively, many people now believe nature itself was the intelligent agent that, through evolution, brought about DNA and all of the innovations needed for life, because that was what was needed. They seem to forget that, by definition, evolution, as defined by its modern Darwinist proponents, is a blind process that has no goals.

By taking control to follow the rules,the system the body uses to control its blood glucose, involving insulin and glucagon, seems to know what it's doing. But, as noted above, regarding having too low of a blood sugar, real numbers have real consequences. Next time, we'll look at what can take place when the system isn't working right and the body experiences too high a level of blood sugar instead.