How appropriate that one of the symbols of the season should be a parasite.
(Also on Sb)
Botanical Wednesday: Festively parasitic
Pharyngula
Evolution, development, and random biological ejaculations from a godless liberal
How appropriate that one of the symbols of the season should be a parasite.
(Also on Sb)
Look with your puny camera eyes! Some new specimens of Anomalocaris, the spectacular Cambrian predator, have been discovered in South Australia. These fossils exhibit well-preserved eyes, allowing us to see that the bulbous stalked balls on their heads were actually fairly typical compound eyes, like those of modern insects.
The cool part of this discovery: the investigators were able to count the density of lenses and estimate how many were present in the intact eye. The number is 16,000 ommatidia in each eye, which is more than a little impressive: to put it in context, Drosophila has about 800. The emphasis on high-resolution vision suggests that Anomalocaris was diurnal predator in shallow water.
Oh, and just in case you’re one of those strange beings who isn’t instantly familiar with what the anomalocarids looked like, here’s a video to remind you.
Paterson JR, García-Bellido DC, Lee MS, Brock GA, Jago JB, Edgecombe GD (2011) Acute vision in the giant Cambrian predator Anomalocaris and the origin of compound eyes. Nature 480(7376):237-40.
(Also on Sb)
I’ve been guilty of teaching bean-bag genetics this semester. Bean-bag genetics treats individuals as a bag of irrelevant shape containing a collection of alleles (the “beans”) that are sorted and disseminated by the rules of Mendel, and at its worst, assigns one trait to one allele; it’s highly unrealistic. In my defense, it was necessary — first-year students struggle enough with the basic logic of elementary transmission genetics without adding great complications — and of course, in some contexts, such as population genetics, it is a useful simplification. It’s just anathema to anyone more interested in the physiological and developmental side of genetics.
The heart of the problem is that it ignores the issue of translating genotype into phenotype. If you’ve ever had a basic genetics course, it’s quite common to have been taught only one concept about the phenotype problem: that an allele is either dominant, in which case it is expressed as the phenotype, or it’s recessive, in which case it is completely ignored unless it’s the only allele present. This idea is so 19th century — it’s an approximation made in the complete absence of any knowledge of the nature of genes.
And the “one gene, one trait” model violates everything we do know about the phenotype and genotype. Every gene is pleiotropic — it influences multiple traits to varying degrees. Every trait is multigenic — multiple genes contribute to the expression of every phenotypic detail. The bean-bag model is totally inadequate for describing the relationship of genes to physiology and morphology. Instead of a bean-bag, I prefer to think of the genome as comparable to a power spectrum, an expression of the organism in a completely different domain. But I wrote about that previously, and I’ll make this explanation a little simpler.
Here’s the problem: you can’t always reliably predict the phenotype from the genotype. We have a skewed perspective on the problem, because historically, genetics has first searched for strong phenotypes, and then gone looking for the genetic cause. We’ve been effectively blind to many subtle phenotypic effects, simply because we don’t know how to find them. When we go the other way, and start by mutating known genes and then looking for changes in the phenotype, we’re often surprised to discover no detectable change. One of the classic examples is the work of Elkins (1990), who found that mutating a neural cell adhesion gene, Fasciclin I, did not generate any gross defects. Mutating another gene, a signal transduction gene called Abelson tyrosine kinase, similarly had no visible effects. Mutating the two together, though — and this is a major clue to how these strange absences of effect could work — did produce gross and obvious effects on nervous system development.
Providing another great example, Steve Pinker examined his own genome, and discovered that his genes said he was predisposed to be red-haired and at high risk for baldness. If you’ve seen Steve Pinker, you know he’s neither.
How can this be? As any geneticist will tell you, the background — the other alleles present in the organism — are important in defining the pattern of expression of a specific gene of interest. One simple possibility is that the genome contains redundancy: that a trait such as adhesion of axons in the nervous system or the amount of hair on the head can be the product of multiple genes, each doing pretty much the same thing, so knocking out one doesn’t have a strong effect, because there is a backup present.
So Steve Pinker could have seen that he has a defective Gene A, which is important in regulating hair, but maybe there’s another Gene B lurking in the system that we haven’t characterized yet, and which can compensate for a missing Gene A, and he has a particularly strong form of it. One explanation for a variable association between an allele and the phenotype, then, is that we simply don’t have all the information about the multigenic cause of the phenotype, and there are other genes that can contribute.
This doesn’t explain all of the observed phenomena, however. Identical twins who share the same complement of alleles also exhibit variability in the phenotype; we also have isogenic animal lines, where every individual has the same genetic complement, and they also show variability in phenotype. This is the problem of penetrance; penetrance is a genetics term that refers to the likelihood that an individual carrying an allele will actually express the phenotype associated with that allele…and it’s not always 100%.
Again, the explanation lies in the other genes present in the organism. No gene functions all by itself; its expression is dependent on a cloud of other proteins — transcription factors, enhancers, chaperones — all of which modulate the gene of interest. We also have to deal with statistical variation in the degree of expression of all those modulatory factors, which vary by chance from cell to cell, and so the actual degree of activation of a gene may follow a kind of bell curve distribution. In the cartoon below, the little diamonds represent these partners; sometimes, just by chance, they’ll be present in sufficiently high numbers to boost Gene B’s output enough to fully compensate for a defective Gene A; in other cases, just by chance, they’re too low in concentration to adequately compensate for the absence.
What the above cartoon illustrates is the concept of developmental noise, the idea that the cumulative total of statistical variation in gene expression during development can produce significant phenotypic variation in the absence of any differences in the genotype. Developmental noise is a phrase bruited about quite a bit, and there’s good reason to think it’s valid: we can see quantitative variation in gene expression with molecular techniques, for instance. But at the same time we have other concepts, like redundancy and canalization, that work to buffer variation and produce reliable outputs from developmental processes, so we don’t have many good examples where we can directly correlate subtle variation at the molecular level with clear morphological differences.
To test that, we have to go to simple animal models (it turns out that Steve Pinker is a rather intractable experimental animal). And here we have a very nice example in the nematode worm, C. elegans. In these experiments, the investigators were dealing with an isogenic strain — the genetic background was identical in all of the animals — raised in a uniform environment. They were looking at a mutant in the gene tbf9, which causes defects in muscle formation, but only 50% penetrance; that is, half the time, the mutants appeared completely normal, and the other half of the time they had grossly abnormal muscle development.
See the big red question mark? That’s the big question: can we trace the abnormal phenotype all the way back to random fluctuations in the expression of other genes in the animal? Yes, they can, otherwise it would never have been published in Nature and I wouldn’t be writing about it now.
In this case, they have a situation analogous to the Gene A/Gene B cartoons above. Gene B is tbx-9; Gene B is a related gene, a duplicate called tbx-8 which acts as a redundant copy. In the experiments below, they knock out tbx-9 with a mutation, and then measure the quantity of other genes in the system using a very precise technique of quantitative fluorescence. Below, I’ve reproduced the entirety of their summary figure, because it is awesome — I just love the idea of being able to count the number of molecules expressed in a developing system. In order to avoid overwhelming everyone, though, I’ll just describe a couple of the panels to give you the gist of the work.
First, just look at the top left panel, a. It’s a plot of the level of expression of the tbx-8 gene over time, where each line in the plot is a different animal. The lines in black are in the wild type animal, with fully functional copies of bothe tbx-8 and tbx-9, and you should be able to see that there’s a fair amount of variation in expression, about two-fold, in different individuals. The lines in green are from animals mutant for tbx-9; it’s messy, but statistically what happens when tbx-9 is knocked out, more tbx-8 gene product is produced.
Panel e, just below it, shows the complementary experiment: the expression of tbx-9 is shown for both wild type (black) and animals with tbx-8 knocked out. Here, the difference is very clear: tbx-9 levels are greatly elevated in the absence of tbx-8. This shows that tbx-8 and tbx-9 are actually tied together in a regulatory relationship where levels of one rise in response to reduced levels of the other, and vice versa.
Now skip over to the right, to panel c. All of the lines in this plot are of tbx-8 expression in tbx-9 mutants, and again you see a wide variation in levels of gene expression. In addition, the lines are color-coded by whether the worm developed normally (blue), or had the mutant phenotype (red). The answer: worms with low tbx-8 levels were more likely to have the abnormal phenotype than those with high levels.
Panel g, just below it, is the complementary analysis of tbx-9 levels in tbx-8 mutants, and it gives the same answer.
Obviously, though, there is still a lot of variability unaccounted for; having relatively high levels of one or the other of the tbx genes didn’t automatically mean the worm developed a wild-type phenotype. There’s got to be something more that is varying. Look way back to the second cartoon I showed, with the little diamonds representing the cloud of transcription factors and chaperone proteins that modulate gene expression. Could there also be correlated variation there? And yes, there is. The authors looked at a chaperone protein called daf-21 that is associated with the tbx system, and found, in mutants for tbx-9, that elevated levels of daf-21 were associated with wildtype morphology (in blue), while lowered levels of daf-21 were associated with the mutant phenotype.
I know what you’re thinking: there isn’t a perfect correlation between high daf-21 levels and wildtype morphology either. But when they do double-label experiments, and take into account both daf-21 and tbx-8 levels in tbx-9 mutants, they found that 92% of the animals with greater than median levels of expression of both daf-21 and tbx-8 had wildtype morphology. It’s still not perfect, but it’s pretty darned good, and besides, it’s no surprise that there are probably other modulatory factors with statistical variation lurking in the system.
What should you learn from this? Developmental noise is real, and is a product of statistical variation in the degree of expression of multiple genetic components that contribute to a phenotype. We can measure that molecular variation in living, developing systems and correlate it phenotypic outcomes. None of this is surprising; we expect that the process of gene expression is going to be a bit noisy, especially in these transcriptional regulators that are present in low concentration in the cell, anyway. But the other cool thing we can observe here is that having multiple noisy systems that interact with each other can produce a more reliable, robust signal and contribute to the fidelity of developmental outcomes.
Burga A, Casanueva MO, Lehner B (2011)
Predicting mutation outcome from early stochastic variation in genetic interaction partners. Nature 480(7376):250-3.
Elkins T, Zinn K, McAllister L, Hoffmann FM, Goodman CS (1990)
Genetic analysis of a Drosophila neural cell adhesion molecule: interaction of fasciclin I and Abelson tyrosine kinase mutations. Cell 60(4):565-75.
(Also on FtB)
I’ve been guilty of teaching bean-bag genetics this semester. Bean-bag genetics treats individuals as a bag of irrelevant shape containing a collection of alleles (the “beans”) that are sorted and disseminated by the rules of Mendel, and at its worst, assigns one trait to one allele; it’s highly unrealistic. In my defense, it was necessary — first-year students struggle enough with the basic logic of elementary transmission genetics without adding great complications — and of course, in some contexts, such as population genetics, it is a useful simplification. It’s just anathema to anyone more interested in the physiological and developmental side of genetics.
The heart of the problem is that it ignores the issue of translating genotype into phenotype. If you’ve ever had a basic genetics course, it’s quite common to have been taught only one concept about the phenotype problem: that an allele is either dominant, in which case it is expressed as the phenotype, or it’s recessive, in which case it is completely ignored unless it’s the only allele present. This idea is so 19th century — it’s an approximation made in the complete absence of any knowledge of the nature of genes.
Usually, I try to accentuate the positive and tell you why other animals are so much more interesting than cats, but today I’m going right for the gutter and showing you why cats are evil. Behold, the cat penis:
You know who else has a penis like that? Satan.
Now you have another reason to get your cats neutered — so they don’t ever use that nightmarish thing.
(Also on Sb)
A few weeks ago, PLoS One published a paper on the observation of preserved chitin in 34 million year old cuttlebones. Now the Institute for Creation Research has twisted the science to support their belief that the earth is less than ten thousand years old. It was all so predictable. It’s a game they play, the same game they played with the soft tissue preserved in T. rex bones. Here’s how it works.
Compare the two approaches, science vs. creationism. The creationists basically insert one falsehood, generate a ludicrous conflict, and choose the dumbest of the two alternatives.
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The Scientific Approach ↓ ↓ find traces of organic material in ancient fossils ↓ Cool! We have evidence of ancient biochemistry! ↓ Science! |
The Creationist Approach ↓ declare it impossible for organic material to be ancient ↓ steal other people’s discovery of organic material in ancient fossils ↓ Cool! Declare that organic material must not be ancient, because of step 1, which we invented ↓ Throw out geology, chemistry, and physics because they say the material is old ↓
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You see, the scientists are aware of the fact that organic materials degrade over time, but recognize that we don’t always know the rate of decay under all possible conditions. When we find stuff that hasn’t rotted away or been fully replaced by minerals, we’re happy because we’ve got new information about ancient organisms, and we may also be able to figure out what mechanisms promoted the preservation of the material.
The creationists start with dogma — in this case, a false statement. They declare
Chitin is a biological material found in the cuttlebones, or internal shells, of cuttlefish. It has a maximum shelf life of thousands of years…
and
Because of observed bacterial and biochemical degradation rates, researchers shouldn’t expect to find any original chitin (or any other biomolecule) in a sample that is dozens of millions of years old—and it therefore should be utterly absent from samples deposited hundreds of millions of years ago. Thus, the chitin found in these fossils refutes their millions-of-years evolutionary interpretation, just as other fossil biomolecules already have done.
But wait. How do they know that? The paper they are citing says nothing of the kind; to the contrary, it argues that while rare, other examples of preserved chitin have been described.
Detection of chitin in fossils is not frequent. There are reports of fossil chitin in pogonophora, and in insect wings from amber. Chitin has also been reported from beetles preserved in an Oligocene lacustrine deposit of Enspel, Germany and chitin-protein signatures have been found in cuticles of Pennsylvanian scorpions and Silurian eurypterids.
So the paper is actually saying that the “maximum shelf life” of chitin is several tens of millions of years. And then they go on to describe…chitin found in Oligocene cuttlefish, several tens of millions of years old. The creationists are busily setting up an imaginary conflict in the evidence, a conflict that does not exist and is fully addressed in the paper.
The creationists do try to back up their claims, inappropriately. They cite a couple of papers on crustacean taphonomy where dead lobsters were sealed up in anoxic, water- and mud-filled jars; they decayed. Then they announce that there’s only one way for these cuttlebones to be preserved, and that was by complete mineralization, and the cuttlebones in the PLoS One paper were not mineralized.
…mineralization—where tissues are replaced by minerals—is required for tissue impressions to last millions of years. And the PLoS ONE researchers verified that their cuttlebone chitin was not mineralized.
Funny, that. You can read the paper yourself. I counted 14 uses of the words “mineralized” and “demineralized”. They state over and over that they had to specifically demineralize the specimens in hydrochloric acid to expose the imbedded chitin. And of course the chitin itself hadn’t been mineralized, or it wouldn’t be chitin anymore! Did the creationists lie, or did they just not understand the paper?
The scientists also do not claim that the chitin has not been degraded over time. They actually document some specific, general properties of decay in the specimens.
β-chitin is characterized by parallel chains of chitin molecules held together with inter-chain hydrogen bonding. The OH stretching absorbance, at about 3445 cm−1 in extant chitin, is diminished in the fossil and shifted to lower wavenumbers, showing that the specimen is losing OH by an as yet undetermined mechanism. The N-H asymmetric stretching vibration is shifted to slightly lower wavenumbers, showing that it is no longer hydrogen bonding exactly as in extant specimens. Changes in the region 2800–3600 cm−1 indicate that biomolecules have been degraded via disruption of interchain hydrogen bonds.
So, yes, the creationists seem to have rather misrepresented what the paper said. Here’s another blatant example of lying about the contents of the paper.
The question they did not answer, however, is why the original organic chitin had not completely fallen apart, which it would have if the fossils with it were 34 million years old…
Actually, they did. A substantial chunk of the discussion was specifically about that question, a consideration of the factors that contributed to the preservation. It was a combination of an anoxic environment, the presence of molecules that interfered with the enzymes that break down chitin, and the structure of cuttlebone, which interleaves layers containing chitin with layers containing pre-mineralized aragonite.
In vivo inorganic-organic structure of the cuttlebone, in combination with physical and geochemical conditions within the depositional environment and favorable taphonomic factors likely contributed to preservation of organics in M. mississippiensis. Available clays within the Yazoo Clay in conjunction with suboxic depositional environment may have facilitated preservation of original organics by forming a physical and geochemical barrier to degradation. One key to the preservation of organic tissues, in particular chitin and chitosan, is cessation of bacterial degradation within environments of deposition. Bacterial breakdown of polymeric molecules is accomplished through activities of both free extracellular enzymes (those in the water column) and ektoenzymes (those on the surface of the microbial cell) such as chitinases. Chitinases function either by cleaving glycosidic bonds that bind repeating N-acetyl-D-glucosamine units within chitin molecules or by cleaving terminal N-acetyl-D-glucosamine groups. These enzymes adsorb to the surface of clay particles, which inactivates them. Strong ions in solution like iron may act in the same manner. Once bound to functional groups within these polymeric molecules, Fe2+ ions prevent specific bond configuration on the active-site cleft of specific bacterial chitinases and prevents hydrolysis, thus contributing to preservation.
Organic layers within cuttlebones are protected by mineralized layers, similar to collagen in bones, and this mineral-organic interaction may also have played a role in their preservation. Specimens of M. mississipiensis show preserved original aragonite as well as apparent original organics. These organics appear to be endogenous and not a function of exogenous fungal or microbial activity. Fungi contain the γ form of chitin not the β allomorph found in our samples. Also, SEM analyses shows there is no evidence of tunneling, microbes, or wide-spread recrystallization of the aragonite. Therefore the chitin-like molecules detected in fossil sample are most likely endogenous. Similar to collagen in bone, perhaps, organics could not be attacked by enzymes or other molecules until some inorganic matrix had been removed.
Like I always say, never ever trust a creationists’ interpretation of a science paper: they don’t understand it, and they are always filtering it through a distorting lens of biblical nonsense. They make such egregious errors of understanding that you’re always left wondering whether they are actually that stupid, or that sleazily dishonest. Or both.
But imagine if the creationists hadn’t screwed up royally in reading the paper, if they had actually found an instance of scientists being genuinely baffled by a discovery that should not be. What if there was actually good reason to believe that chitin could not last more than ten thousand years?
Then the only sensible interpretation of this observation of 34 million year old chitin would be that the prior estimation of the shelf-life of chitin was wrong, and that it could actually last tens of millions of years. What the creationists want to do is claim that that minor hypothetical is actually correct, and that instead the entirety of nuclear physics, geology, radiochemistry, and modern cosmology is wrong. On the one hand, uncertain details about the decay of one organic molecule; in the other, entire vast fields of science, already verified, and with complex modern technologies built on their operation…and which hand would the creationists reject? The trivial one, of course.
I’m leaning towards “stupid” as the explanation for their bad arguments.
Oh, after I started this dissection, I discovered someone had already beaten me to it: here’s another analysis of the creationist misinterpretations.
(Also on Sb)
I will never forgive Leon Lederman for calling the Higgs boson the “god particle”. It’s fueled decades of unjustified patronizing nonsense from theologians, and the latest is Alister McGrath, who babbles obliviously about it.
Science often proposes the existence of invisible (and often undetectable) entities – such as dark matter – to explain what can be seen. The reason why the Higgs boson is taken so seriously in science is not because its existence has been proved, but because it makes so much sense of observations that its existence seems assured. In other words, its power to explain is seen as an indicator of its truth.
There’s an obvious and important parallel with the way religious believers think about God. While some demand proof that God exists, most see this as unrealistic. Believers argue that the existence of God gives the best framework for making sense of the world. God is like a lens, which brings things into clearer focus. As the Harvard psychologist William James pointed out years ago, religious faith is about inferring “the existence of an unseen order” in which the “riddles of the natural order” can be explained.
The parallel breaks down hard, though. Yes, the Higgs boson is a satisfying theoretical construct with much power to explain. But notice that mathematical beauty was not enough: the physicists of the world, from over 100 countries, gathered and spent over $9 billion to build the largest scientific instrument in the world to test the hypothesis. Faith was not enough.
In contrast, you couldn’t convince a Baptist and a Mormon to get together and chip in $1.98 to test their god. Because they don’t have the slightest idea how to do it, and wouldn’t be interested if they did.
That’s the real lesson to be learned from the science: you have to do the test.
I know how I’m going to spend the entirety of my Christmas break: preparing to teach my new Cancer Biology course. And since I’m going to be dwelling on cancer for the next month or so, I think it’s only fair that my students and any passers-by should also get a faceful of the stuff. So here are the texts I’ve settled on for the course:
Weinberg’s Biology of Cancer
Skloot’s Immortal Life of Henrietta Lacks
Mukherjee’s The Emperor of All Maladies
There will also be a few papers assigned throughout the term, but that ought to get everyone started on a good long depression.
