I thought that Vox and I were in pretty substantive agreement when it comes to distinguishing between the science of evolution and the ideologically-motivated misapplication of that science. Curious, then, that he has expended several thousand words over at his site as to which Nazi wore which belt buckle, or whether the Soviets were 'inspired' by Darwin. I can't blame Vox entirely for returning to this line of questioning, since it suits his interests and his strengths: he is, after all, something of a professional when it comes to pushing ideology.
But all of that stuff has nothing to do with the question of what the science actually is, of whether "TENS is the only serious game in town at the moment." (Which is is!) Vox admits that he is "in no way opposed to its continued refinement and application in the field of biology," and wants people to know he's never been opposed to it. Well, Vox, let me say that you've got a funny way of showing it. I'll give you the benefit of the doubt, though, since I'm pretty sure that most of your snide remarks are really at the expense of Dawkins and other committed evolutionists, rather than the actual science.
And----speaking of the actual science----don't you think it's time we focused on it? Vox continues to argue that what he calls 'backtesting' casts doubts on the reliability of TENS, with respect to my posts on the chimpanzee chromosome:
Now, look at this wording: "the first SUGGESTION that... MIGHT'VE BEEN PRODUCED" is not at all equivalent to the "testable prediction"
Oh, Vox, of course it is. Lejeune et al suggested telomeric fusion as a possible explanation back in 1973. That's a hypothesis. That hypothesis clearly implies that signatures of the fused telomeres and that of an inactivated centromere, if they still exist, should be found in the DNA sequence (which at the time was unknown). That's a prediction (actually two predictions) that were verified by later research. No one who actually understands this research would disagree with this claim. Not a soul.
It's entirely possible that the "testable prediction" was made prior to the tests, but we still haven't seen proof of it.
Vox, you are just playing word games here rather than addressing the science on its own merits. Back in 1973, LeJeune and other researchers proposed a radical hypothesis (telomeric fusion) to explain the banding patterns they saw. Subsequent analysis of the DNA sequence could've provided evidence against this interpretation. The banding patterns which seemed to suggest the fusion of two separate chromosomes could've been artifacts of other types of chromosomal change. The sequences, when examined, could've failed to line up with homologous sequences in the two chimpanzee chromosomes. The presence of pericentromeric regions within chromosome #2, the signature of an ancestral chromosome's inactivated centromere, could've failed to appear upon closer investigation.
None of those things happened. Why do you think that is? Please try to form an answer that refers to the science, rather than another attempt at derailing the clear implication of this line of work. Do you want, as you said before, to learn something from this 'debate' about the real science, or do you just want to play a game of semantic dodge ball?
9/02/2007
VOX DEI-BATE #11: LET'S TALK ABOUT THE SCIENCE
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I don't want to appear smug but, in my first comment on your blog, I predicted that he would adopt a number of tactics, one of which was that "where he can't raise "mathematical" objections, he'll usually resort to semantics to confuse the issue as much as possible." Without wishing to appear smug, I would just like to say that I called that one pretty well. Let's roll!
Billy: you did predict that this would happen. Let's see if Vox stonewalls on this point, or if he finally engages on the basis of the science.
And if not, I'll use your earlier post as an example of a testable prediction!....:)
Hi Scott,
I was curious and spent about half an hour looking for other examples of tested predictions related to evolution. I've included a few that I found below, that you might (or might not) determine are useful in providing additional examples. I was surprised by how easy it was to find these only using Google. It suggests to me that someone else interested in finding such examples who has the time to devote and access to a broader and deeper set of scientific journals could discover a very large number of prediction/test examples, were they to actually look.
The last example re: "experimental evolution" seemed particularly interesting.
Wheat is an ancient crop of the Middle East. Three species exist both as wild and domesticated wheats, einkorn, emmer, and breadwheat. Archeological studies have demonstrated that einkorn is the most ancient and breadwheat appeared most recently. To plant biologists this suggested that somehow einkorn gave rise to emmer, and emmer gave rise to breadwheat (an hypothesis). Further evidence was obtained from chromosome numbers that showed einkorn with 14, emmer with 28, and breadwheat with 42. Further, the chromosomes in einkorn consisted of two sets of 7 chromosomes, designated AA. Emmer had 14 chromosomes similar in shape and size, but 14 more, so they were designated AABB. Breadwheat had chromosomes similar to emmer, but 14 more, so they were designated AABBCC. To plant biologists familiar with mechanisms of speciation, these data, the chromosome numbers and sets, suggested that the emmer and breadwheat species arose via hybridization and polyploidy (an hypothesis). The Middle Eastern flora was studied to find native grasses with a chromosome number of 14, and several goatgrasses were discovered that could be the predicted parents, the sources of the BB and CC chromosomes. To test these hypotheses, plant biologists crossed einkorn and emmer wheats with goatgrasses, which produced sterile hybrids. These were treated to produce a spontaneous doubling of the chromosome number, and as predicted, the correct crosses artificially produced both the emmer and breadwheat species. No one saw the evolution of these wheat species, but logical predictions about what happened were tested by recreating likely circumstances.
[cite]
The cold-climate hypothesis for evolution of viviparity in squamates predicts a
correlation between reproductive mode, altitude and latitude. I tested this
prediction in horned lizards within a phylogenetic context. I first determined
whether all viviparous species were monophyletic using Monte Carlo
simulations. Secondly, I tested for presence of phylogenetic signal using
randomization tests. Thirdly, I analysed relationships between reproductive
mode and minimum, midpoint, and maximum altitudes and latitudes by
computing conventional correlations and phylogenetically independent contrasts.
[cite]
Using an appropriately designed and replicated study of a latitudinal influence on rates of evolution, we test the prediction by K. Rohde [(1992) Oikos 65, 514–527] that the tempo of molecular evolution in the tropics is greater than at higher latitudes. Consistent with this prediction we found tropical plant species had more than twice the rate of molecular evolution as closely related temperate congeners.
[cite]
Under the appropriate set of conditions, Alexander predicted, evolution ought to produce a eusocial vertebrate, even though eusociality in the naked mole-rat (or any other vertebrate) was unknown at the time.
[...]
Alexander based his answer on his understanding of the selective forces involved in the evolution of insect eusociality and hypothesized a eusocial vertebrate. He created a 12-part model for a eusocial vertebrate, based on this body of theory. He had no idea that a mammal with these characteristics existed.
[...]
Jarvis had studied the ecology and physiology of naked mole-rats but at that time nothing was known about their social system. Subsequent field and laboratory observations have confirmed that they are in fact eusocial, as Alexander´s model had predicted, and that the other elements of his model are accurate as well ...
[cite]
The successful spread of invasive plants may result from an evolutionary shift in resource allocation from defence to growth due to release from enemies, as proposed by the ‘evolution of increased competitive ability’ hypothesis (EICA). The crucifer Lepidium draba was used to test this hypothesis, measuring growth and levels of glucosinolates and myrosinase of leaves as constitutive defence parameters.
[cite]
Evolutionary theory predicts the impact of a difference in extrinsic mortality on intrinsic mortality rates (hence, lifespan) and on growth, maturation, body size, and reproduction. When extrinsic mortality rates increase, they lower the probability of survival to a given age and cause the strength of selection to decline faster with age, making an increase in intrinsic mortality rates with age “more affordable” or “less avoidable.” From this concept follows a central prediction of the evolutionary theory of aging: Higher extrinsic mortality rates should lead to higher intrinsic mortality rates and a decrease in lifespan ...
[...]
Recently, a new tool has been exploited to test such predictions: experimental evolution. In contrast to artificial selection, in which the experimenter determines which trait is selected, in experimental evolution, the experimenter creates the conditions under which a prediction should hold and lets the evolving population determine with which traits the problem will be solved. This approach has yielded important insights with bacteria, algae, poeciliid fish, and temperature adaptation in flies. It succeeds because evolution is more rapid than until recently was expected.
[...]
This experiment tested and confirmed the prediction that higher extrinsic mortality rates lead to the evolution of higher intrinsic mortality rates, something that had been done previously (25–31), but never before with such a realistic and precisely measured difference in mortality regimes and with such precise control of both adult and juvenile population densities. It also confirmed all of the major predictions of life-history theory in a case in which mortality rates were known precisely and where the confounding effects of density variation in both adults and larvae were excluded.
[cite]
Zzrox: That's just awesome. I'd forgotten entirely about the example of the naked mole rat. I think I'll dust that one off and post about it if anyone whines I've only one example.
And, yeah, any one who is really interested in actually looking for predictions made by evolutionary biologists can find them for themselves, I think. Kinda makes ya wonder, don't it?
Scott
I love your attempts to deal with the shifting sands of the Vox thing. It isn't a debate it is you trying to talk to people with their hands over their ears going "naaah naah".
They will not listen to reason and evidence is something they cannot countenance if it goes contrary to the dogma that directs their life.
You are a patient dude but sometimes you have to recognise an ambush with no way out. The people who frequent Vox's site are not open to reason they are dogmatists and as such have more in common with the people they decry than they care to admit. Trying to reason with them is like peeing in the wind.
Trying to reason with them is like peeing in the wind.
(grinning) What interests me is which direction the stream flows after being released. What I observe is that, if the wind blows one way, no matter what they say, they are clearly religiously-motivated creationists. If the wind blows another way, some other interpretation may be true, but in the meantime we can follow the spattered trail and demonstrate how their arguments proceed from dogma, rather than empirical investigation.
You would be interested to read some of his posts from March and April. He doesn't think evolutionary biology is an actual science. And if you read the comments he makes in his posts, he thinks engineers make all the real progress in society anyways. So not only is evolution not science, but even if it were it would still be useless. So you are essentially arguing against a brick wall. An intellectually dishonest brick wall that is now, confronted with overwhelming evidence, trying to backpeddle from the position he took earlier in the year. You are an artful debater, but I wouldn't waste my time.
Next thing you know he will try to argue that the prediction to results ratio will be too low to be useful, despite physicists' predictions about subatomic particles also having a dreadfully low accuracy rate.
I think I'll dust that one off and post about it if anyone whines I've only one example.
If it's mathematical-style evidence we want, shouldn't numbers of examples count?
I'm a bit perplexed why you're letting Vox off so easy on this. We have catalogued -- what -- a million species? Three million?
Out of the millions of species found on Earth, not one has been found yet that doesn't fit the modern evolution theory. Not one. A while back another "new" rat was identified from Southeast Asia. Without knowing anything more about it, we can make a thousand very accurate predictions about the creature, its morphology, its size, its probable diet, and so on.
Is there a species on Earth known to science that doesn't have an ancestor in fossils?
And have you slipped in the odd whale anklebone (whales have ankles? Yes, Virginia, they do) predicted by the molecular biologists, that the paleontologists later found?
And don't forget sympatric illustrations of evolution by natural and sexual selection, especially those perfect creationism-crushing models, ring species.
Mathematics? There are between one and three million examples of evolution as Darwin described it, and none contrary. Those are pretty staggering numbers, to people of any sense.
Ed Darrell:
Out of the millions of species found on Earth, not one has been found yet that doesn't fit the modern evolution theory. Not one.
Recent research on Sea Anemone Provides a New View of Animal Evolution notes:
The newly decoded DNA of a few-centimeter-tall sea anemone looks surprisingly similar to our own,
The work is truly stunning for its deep evolutionary implications,
The draft genome is already producing many surprises. Among the anemone's 18,000 or so protein-coding genes, the researchers have identified 7766 that are also present in bilaterians. Those shared genes represent the knowable part of the ancestral gene set. Three-quarters of the genes turn up in all three major animal groups examined, humans among them, but 1292 have been lost in the fruit fly and the nematode.
One of the big surprises of the anemone genome, says Swalla, is the discovery of blocks of DNA that have the same complement of genes as in the human genome. Individual genes may have swapped places, but often they have remained linked together despite hundreds of millions of years of evolution along separate paths, Putnam, Rokhsar, and their colleagues report.
Moreover, the anemone genes look vertebratelike. They often are full of noncoding regions called introns, which are much less common in nematodes and fruit flies than in vertebrates. And more than 80% of the anemone introns are in the same places in humans, suggesting that they probably existed in the common ancestor. "The work presents a missing piece of the puzzle, which people studying intron evolution have been searching for in the past few years," says Majewski. "They present a strong validation for an intron-rich ancestor," he says.
This implies that even very ancient genomes were quite complex and contained most of the genes necessary to build today’s most sophisticated multicellular creatures.
Here's the question for "modern evolution theory" (keep in mind that in an "intron-rich ancestor", introns are not expressed.)
So, how did random mutation and natural selection create the complex genes ultimately needed by complex bilaterians but dropped from lesser complex organisms, hundreds of millions of years in advance of those more complex organisms being naturally selected for survival?
How can natural selection favor random mutations of genes that were not being expressed?
Here's the question for "modern evolution theory" (keep in mind that in an "intron-rich ancestor", introns are not expressed.)
Right on. Let's hear it.
....how did random mutation and natural selection create the complex genes ultimately needed by complex bilaterians but dropped from lesser complex organisms, hundreds of millions of years in advance of those more complex organisms being naturally selected for survival?
Three potential conceptual missteps here.
(1) Natural selection is not involved in the creation of genetic variation, only in the elimination of those variants which, in a given environment, reduce an organism's reproductive success. It is mutation (AND sexual recombination AND 'crossing-over' AND population growth AND other things) that is constantly generating variation.
<2> Evolution has no locally-proscribed 'direction' towards either simplicity or complexity. It's a question of what genetic 'solutions' to the local environmental 'problems' are available to the local population, and what is the relative reproductive success associated with each 'solution.'
<3> It is a mistake to assume that only the common-place, everyday production of genetic variation via the above processes is sufficient to account for every aspect of all macroevolutionary events. Biologists today acknowledge that we see evidence for major reorganizations of the genome, as in the example of human chromosome #2, and telomeric fusion is just one way that such reorganizations are effected. These processes could be described as meta-variatonal: they do not necessarily effect what genes are present so much as they act as 'switches' to turn the genes 'on' or 'off'.
How can natural selection favor random mutations of genes that were not being expressed?
It can't. No one is arguing that it can. Introns may not code for protein, but they are believed in many cases to carry regulatory functions for those parts of the genome which are expressed. Natural selection selects against the presence of regulatory functions that adversely affect the organism's ability to pass on its genes in a given environment, even in the absence of direct phenotypic effects; if those regulatory functions are not critical in the above sense, however, mutations that might impair or alter function could accumulate, and the evidence for this are the many pseudogenes that have already been described in the literature. I have to confess I much prefer Carroll's term 'fossil gene' for such, for obvious reasons. Read 'The Making of the Fittest' for a popularization to help make sense out of all this. You just quoted a summary of work in the primary literature, and I don't think it's giving you enough context to address your conceptual misgivings.
Scott Hatfield:
You just quoted a summary of work in the primary literature, and I don't think it's giving you enough context to address your conceptual misgivings.
Ok, the primary paper is Sea Anemone Genome Reveals Ancestral Eumetazoan Gene Repertoire and Genomic Organization.
Permit me to rephrase my question in light of the paper and your corrections.
It is mutation (AND sexual recombination AND 'crossing-over' AND population growth AND other things) that is constantly generating variation.
Except there is little variation in the sea anemone Nematostella vectensis over several hundred million years and little variation compared to the orthologous human genes:
"Comparison of Nematostella genes to those of other animals reveals that the ancestral eumetazoan genome must have been intron-rich, with gene structures closely resembling those of modern vertebrate and anemone genes. Introns that are shared between Nematostella and vertebrates and/or other bilaterians are most parsimoniously interpreted as conserved ancient eumetazoan introns (40). Not only are the numbers of exons per gene similar between Nematostella and vertebrates, but the precise location and phase (i.e., the positioning of the splice sites relative to codon boundaries) of introns are also highly conserved between the anemone and human (Fig. 2A).Within alignable regions, nearly 81% of human introns are found in the same position and phase in Nematostella; conversely, 82% of the anemone introns are found in orthologous positions in human genes (32)."
"The conserved linkage is extensive, and it accounts for a large fraction of the ancestral eumetazoan set. Of the 4402 ancestral eumetazoan gene families represented in the largest anemone scaffolds and human segments (i.e., in the genomic regions large enough to permit statistically significant analysis and therefore eligible for consideration in our analysis), more than 30% (1336) participate in a conserved linkage group."
"Within such human segments, typically 40 to 50% of eumetazoan-derived genes have counterparts in syntenic Nematostella segments, and vice versa. This is a notable total, given that any chromosomal fusions and subsequent gene order scrambling on either the human or Nematostella lineage during their ~700 million years of independent evolution would attenuate the signal for linkage."
But there were new genes created as well:
"The remaining 20% (1584) of the ancestral eumetazoan gene set comprises animal novelties that were apparently “invented” along the eumetazoan stem. The mechanism for the creation of “new” genes is obscure (57) but may involve gene duplication followed by bursts of rapid sequence divergence (thus masking the similarity with sister sequences) and/or de novo recruitment of gene and/or noncoding fragments into functional transcription units. We classified these eumetazoan novelties into three categories based on their origin (Fig. 4A)"
"The eumetazoan ancestor possessed more than 1500 genes that are apparently novel relative to other eukaryotic kingdoms."
And genes were lost in other lineages:
"In contrast, the fruit fly and nematode model systems have experienced extensive gene loss (18), intron loss (30), and genome rearrangement."
"We found 1292 eumetazoan gene families that had detectable descendants in anemone and at least two of the three vertebrates, but that appeared to be absent in both fruit fly and soil nematode. This indicates that they were either lost or highly diverged in both of these model protostomes, extending the list of such genes found in EST studies (17, 18)."
So, rephrasing my questions now:
How does the modern theory of evolution (TENS?) account for Nematostella to seemingly "out of the gate" possess so many unexpressed and conserved characteristics that would not be expressed until several hundred million years later in bilaterians (which would then still survive natural selection) ? i.e, how were its genes so successful so far in advance of being fully expressed?
Scott, you wrote earlier:
Natural selection is not involved in the creation of genetic variation, only in the elimination of those variants which, in a given environment, reduce an organism's reproductive success.
So NS is ruled out for creating new genes and little was eliminated (certainly little that was not later expressed in bilaterians) but much was selected out from fruit fly and nematode, so there was selective pressure on those genes and introns but not adverse to Nematostella, no?
It is mutation (AND sexual recombination AND 'crossing-over' AND population growth AND other things) that is constantly generating variation.
But that seems largely ruled out as Nematostella underwent little variation over several hundred million years, no?
Evolution has no locally-proscribed 'direction' towards either simplicity or complexity. It's a question of what genetic 'solutions' to the local environmental 'problems' are available to the local population, and what is the relative reproductive success associated with each 'solution'.
Seemingly, there was little role for evolution as you point out it is indifferent to simplicity vs complexity and Nematostella had a fairly static 'successful solution' for several hundred million years, right?
And you point out that natural selection can't [favor genes in an intron-rich ancestor that were not expressed] but that NS selects against the presence of regulatory functions that adversely affect the organism's ability to pass on its genes in a given environment.
Except again that Nematostella seemingly was unaffected by any adverse selective pressure (unlike the fruit fly and nematode) as it quite clearly conserved and passed on it genes with little variation or impairment for several hundred million years, so again NS seems ruled out as significant factor.
The paper also concludes with:
"Nematostella and its genome provide a platform for testing hypotheses about the nature of ancestral eumetazoan pathways and interactions, with the use of the basic principle of evolutionary developmental biology: Processes that are conserved between living species were likely functional in their common ancestor."
So, how does "modern evolution theory" or TENS explain Nematostella's initial collection of successful and likley functional but unexpressed bilaterian genes and introns, and their conserved and fairly static continued success for several hundred million years, with natural selection and mutation largely on the sidelines, little variation in play, and evolution being indifferent to simplicity, complexity and an intially and ongoing successful solution?
(ps, I won't likely be participating further til this weekend...)
OT request: can you enable blockquote tags so text can indented in posts?
I think you're reading too much into this article. There's nothing revolutionary about the finding you're describing. We recognize many strongly conserved elements in the non-coding DNA, genetic switches that are turned 'on' in some lineages and turned 'off' in others. The Carroll book I refer to describes them somewhat romantically as 'immortal genes' because of their conservation.
I suspect that what you're trying to argue is that all that variation in the lineage, or at least all the capacity for variation, was somehow 'hard-wired' in advance by the Generator Of Diversity, rather than (as biologists hold) being the result of stochastic processes.
If so, it just won't wash. The soft-bodied sea anemones don't have an extensive fossil history, but they are hardly basal to the metazoa. The oldest ones we know are Middle Cambrian, and (as you should be aware) the origin of the metazoa is, at the very least, more than 100 million years prior to that. So there was plenty of time for the strongly-conserved 'immortal genes', plenty of time for the non-coding regulatory elements to become fixed in the LCA of all metazoa.
Doesn't rule out the existence of the Generator Of Diversity, of course. It just means that we can't derive said existence from the facts of diversity. Again, I highly recommend Carroll. You're flailing about in technical literature that biologists who aren't specialists have to do their homework to understand, and if you aren't a biologist, the learning curve is even steeper. Why not get the context from someone who is eminent in the field, and a gifted presenter?
Scott Hatfield:
We recognize many strongly conserved elements in the non-coding DNA, genetic switches that are turned 'on' in some lineages and turned 'off' in others. The Carroll book I refer to describes them somewhat romantically as 'immortal genes' because of their conservation.
But my question went to how does TENS explain/predict/require their formation, conserved and turned 'off', several hundred million years in advance? Feel free to paraphrase Carroll if he has addressed not their recognition, but the evolutionary theory of their initial formation.
I suspect that what you're trying to argue is that all that variation in the lineage, or at least all the capacity for variation, was somehow 'hard-wired' in advance by the Generator Of Diversity, rather than (as biologists hold) being the result of stochastic processes.
Well, it is more than variation or capacity for variation. The conserved (unvarying) genes were there several hundred million years in advance. I was asking how evolution theory explains stochastic processes that selected ('hard-wired' in advance if you prefer) for that, given the unexpressed nature of the genes. While there may be other scientific explanations as more comes to light, I was asking for the TENS explanation as best we understand the evidence today.
So there was plenty of time for the strongly-conserved 'immortal genes', plenty of time for the non-coding regulatory elements to become fixed in the LCA of all metazoa.
You can postulate adequate time for their becomeing fixed, but the question is really where is the evidence of LCA's that lack those 'immortal genes'? Where is the evolution of those 'immortal genes', not just when they may have become fixed, but where were they unfixed and absent in an LCA?
You're flailing about in technical literature that biologists who aren't specialists have to do their homework to understand, and if you aren't a biologist, the learning curve is even steeper.
That doesn't sound like something you tell your students. I don't mind flailing, homework, or steep learning curves, and this is a blog, and comments are invited, though there is no obligation for anyone to answer anybody.
Why not get the context from someone who is eminent in the field, and a gifted presenter?
As previously noted, I don't regard "popularizations" as they are profit/market oriented, overly broad and sensational, and not peer reviwed, nor can I ask it the specific questions I prefer (not that I often email questions to researchers anyway, though I have at times).
(sorry for the drive-by, but gotta run)
I was asking how evolution theory explains stochastic processes that selected ('hard-wired' in advance if you prefer)
No, no, no. I don't prefer. 'Hard-wired' implies design. We don't do teleological thinking in science, because that appeals to a non-falsifiable claim. I'm saying that evolutionary theory, as science, explains the apparent design/functionality/conservation etc. of these 'immortal genes' in the same way it explains all features of an organism: either as a contingent event, a result of chance alone, or else a stochastic process in which variations with less fitness are continually culled from the population.
You ask, in effect, where these strongly-conserved introns were before the metazoan lineage? Well, I am sure the state of our knowledge on that point is hazy, but that is not evidence for the proposition that these elements were designed, much less that the design work was future design work, as if the Generator Of Diversity was 'planning ahead.'
Remember, this is non-coding DNA that functions as a regulatory element, genetic switches that turn 'on' or 'off'. These are generic types of instructions; they aren't coding for any gene in particular! So it's fundamentally incorrect to presume that their antiquity speaks to the apparent design of present organisms---and you should be aware that different organisms use these genetic 'switches' in different ways. None of this is evidence for 'advance planning.' As always, evolution is a process of tinkering, working with the various components present at any given moment. The genetic switches are heavily-conserved not because they turn any particular expressed gene 'on' or 'off' at any particular moment in a particular lineage; rather, it is their general usefulness, in that they can be coopted for a variety of usages by all sorts of metazoans, that leads to their nigh-universal conservation.
Read Carroll. Please.
Scott Hatfield:
The Carroll book I refer to describes them somewhat romantically as 'immortal genes' because of their conservation. Again, I highly recommend Carroll. ... Read Carroll. Please.
If I wanted a romatic explanation, I'd by a Harlequin novel. Carroll's "immortal genes" do not apply to this discussion:
Carroll coined the term "immortal gene" as a short hand for those genes that underwent purifying natural selection and have been conserved across domains of life, more scientifically those genes whose ratio of nonsynonymous to synonymous substitutions is observed to be about 1:3. A ratio of nonsynonymous substitutions to synonymous substitutions < 1 indicates purifying selection or structural constraints.
1) Because Carroll alludes to purifying selection in "immortal genes", the nonsynonymous and synonymous substitutions occurr within exons (single nucleotide polymorphism which leads to the same (synonymous) or different (nonsynonymous) polypeptide sequence, which polypeptide sequences are the resuts of transcription, i.e. gene expression), so the observed "immortal gene" substitution ratio 1:3 is for exons or expressed genes. We are discussing why unexpressed genes were conserved for several hundred million years, not expressed genes.
2) Regardless, purifying selection does not explain how Nematostella's unexpressed genes were first formed with so much unexpressed (i.e. naturally non-selected) and seemingly needless complexity. How natural selection demonstrates conservation in expressed genes, maybe, but "immortal genes" are silent on the issue of how or why unexpressed genes were formed initially.
Lastly, no I'm not going to waste my time with popularizations. We've been over this. Carroll has written two books and I'm told in neither book does he cite his assertions with any scientific findings or evidence. There is no, zip, nada, zilch, bupkis evidence or science to be had from a popularization, not even Carroll's. Imagine my irritation with you, personally, had I wasted the time and money searching Carroll's book for an explanation to the topic at hand, only to find the "immortal gene" gene was neither applicable nor sourced.
Seriously Scott, you titled and argued in this thread about discussing science, you further criticized my quotes from a popularized press release for a primary paper, but then when I cite the primary paper you accuse me of flailing around in the technical literature and you then deflect back to popularizations! And I tried rephrasing in terms you suggested, and you've deflected those as well.
Are we gonna discuss the science that does or doesn't underly TENS or are we just gonna drag out dueling popularizations? Pick a position and stick with it.
I'm saying that evolutionary theory, as science, explains the apparent design/functionality/conservation etc. of these 'immortal genes' in the same way it explains all features of an organism: either as a contingent event, a result of chance alone, or else a stochastic process in which variations with less fitness are continually culled from the population.
Except that immortal genes are expressed genes. If you insist on including unexpressed genes, then get Carroll to explain the substitution ratios and purifying selection for unexpressed genes (should make for great romatic pulp).
And what contingency exists for genes several hundred million years in advance of their expression? What is the mechanism by which an unexpressed gene has a contingency? Contingent on what? If you're going to argue contingent on non-coding regulatory sequences, fine. But then you'll be arguing much more of the genome has contingencies than the 95+ percent attributed to 'junk'. Which is it? Junk or contingent?
And "chance" and "stochastic process" are synonyms, both ambiguous imprecise allusions to varying degrees of probability (or improbability). If you insist on arguing chance and probability in the formation of unexpressed genes, at least cite whatever numbers and the mechanisms support your arguement (scientifically please, not romantically).
We don't do teleological thinking in science, because that appeals to a non-falsifiable claim.
And where is the falsifiability in your appeals to romantic "immortal genes", unstated contingencies, chance and stochastics, and hazy knowledge? And your repeated strawmen about the "Generator Of Diversity" is wearing thin. I didn't raise those arguments, you are. I asked "how does TENS explain/predict/require their formation, conserved and turned 'off', several hundred million years in advance?" If your students asked the same question would you raise the same strawmen?.
I didn't ask how the "Generator Of Diversity" did it. I didn't ask how any expressed genes were conserved, I didn't ask ... well I'm sure you'll provide many more answers to what I've not asked.
As for the science I have asked, I'm not holding my breath.
Scott Hatfield:
I previously overlooked your statement:
So it's fundamentally incorrect to presume that their antiquity speaks to the apparent design of present organisms---and you should be aware that different organisms use these genetic 'switches' in different ways. None of this is evidence for 'advance planning.'
Agreed, antiquity alone of non-coding DNA does not argue "apparent design of present organisms" nor is "evidence of advance planning" (to reuse your phrasing).
Recall, however this all started with Ed Darrell's challenge: "Out of the millions of species found on Earth, not one has been found yet that doesn't fit the modern evolution theory. Not one."
Well, neither natural selection nor "immortal genes", nor stochastic processes explain the antiquity, plus the complexity, plus the orthology of these introns with present organisms, so I still haven't seen modern evolution theory explain them either.
Scott Hatfield:
A final point about the 'antiquity' implications: they are two fold:
1) The unexpressed complexity was conserved for several hundred million years.
2) But that same unexpressed complexity didn't have all the precambrian to 'evolve' because it had to follow the formation of eukaryotes which were about 1,500 Mya.
Up to the cnidarian-bilaterian split at 650-1,000 Mya then leaves 500-850 M years for the above noted complexity to 'evolve' from eukaryotes by stochastic processes.
I sense irritation. Look, guy, I'm not trying to be patronizing. You're making what you think is a good argument. I'll try to answer it, but the point about urging you to read Carroll is so you can place that argument in context. You are clearly attempting to read things into the primary literature that the authors themselves almost certainly did not intend. If they had, those implications would've ended up in the discussion section. Instead, what I observe are references to the very processes that Carroll’s book discusses, items which I am showing in bold:
(Pg. 90) “The eumetazoan genes of ancient eukaryotic ancestry are themselves descended from ~5148 eukaryotic progenitors by nearly 1000 gene duplications along the eumetazoan stem.....”
(Pg. 90) “The mechanism for the creation of “new” genes is obscure, but may involve gene duplication followed by bursts of rapid sequence divergence (thus masking the similarity with sister sequences) and/or de novo recruitment of gene and/or non-coding fragments into functional transcription units.”
(Pg. 90) “...the novel domains they contain were evidently invented (or evolved into their recognizable animal form) and coupled to more ancient domains on the eumetazoan stem. For example, Notch proteins have two Notch domains found only in metazoans...”
(Pg. 91) “...Individual “new” genes are by themselves unlikely to bring about the suite of features needed to evolve animal characteristics from unicellular organisms. Rather, we expect that to generate organismal novelty, such new genes must be integrated with other novel and existing genes to evolve expanded or modified biochemical pathways and/or regulatory networks.”
(Pg. 92) “A general trend in the evolution of signaling pathways may have been the co-option of cytosolic signaling components into pathways that could be regulated by newly invented ligands and receptors.”
(Pg. 94) “Unfortunately, we cannot read from the genome the nature of its gene and protein-regulatory interactions and networks. This is particularly vexing, as it is becoming clear—especially given the apparent universality of the eumetazoan toolkit—that gene regulatory changes can also play a central role in generating novelties, allowing co-option of ancestral genes and networks to new functions.”
See, Carroll explains this stuff with far greater verve and wisdom than I can muster, and he places it in a broader context than the paper you’re trying to hang your hat on. The authors of this paper clearly have that broader context, as some of the above passages (“new” genes, for example!) show. So, instead of being offended that I refer you to a popularization, please consider the possibility that the line of reasoning you’re attempting to develop will need to be nested in that broader context in order to find a wider audience. You’re a bright guy, doubtless, but you’re also a non-specialist who is attempting to directly grapple with the primary literature in order to build a case for a decidedly non-standard interpretation of the data.
Now for some potential conceptual missteps on your part. I say ‘potential’ because there is always a possibility that I am misreading you and I ask your pardon in advance if that’s the case. You write:
“We are discussing why unexpressed genes were conserved for several hundred million years, not expressed genes.”
You may be discussing that, but I kind of doubt that Putnam et al are discussing that, and I certainly don’t think that follows from the article in question. You appear to have stubbed your conceptual toe here. It is not so much that genes lay ‘dormant’or unexpressed, but that the modular regulatory networks that are today involved in the expressions of those genes were likely doing different things in the past. Sure: the introns involved can not be said to be ‘expressed’ in the sense that an exon is, in that they are not coded as protein. But it is manifestly true that they are conserved. Lineages that lose the ability to combine (or recombine) these modules lose a great deal of plasticity in terms of the permissible range of responses to the environment and would be at a selective disadvantage compared to those that retained said plasticity, even if they are not ‘expressed’ in a particular way as a particular trait for many generations. Again, what is being conserved is not necessarily any particular pattern of expression, but the general capacity to build modular networks. To the best of my knowledge, no one is claiming that ‘unexpressed genes were conserved.’ If that’s your understanding, I think you’re misreading the data. If I’m wrong on that point, if someone in a peer-reviewed publication has actually suggested otherwise, I’d be delighted to look at that.
Regarding Carroll, you wrote: “Carroll has written two books and I'm told in neither book does he cite his assertions with any scientific findings or evidence.”
Who told you that? You’re out on a limb there, pal. Carroll repeatedly cites his own work as well as others in ‘Endless Forms Most Beautiful’. ‘The Making of the Fittest’ relies more heavily on the work of others, and it’s more user-friendly than the other book, but there’s plenty of evidence presented, with plenty of citations. The term ‘popularization’ doesn’t have to mean either ‘dumbed-down’ or ‘lacking in integrity.’
“Seriously Scott, you titled and argued in this thread about discussing science, you further criticized my quotes from a popularized press release for a primary paper, but then when I cite the primary paper you accuse me of flailing around in the technical literature and you then deflect back to popularizations! And I tried rephrasing in terms you suggested, and you've deflected those as well..”
The title doesn’t refer to your honest attempts to engage the literature, but to the fact that Vox and his syncophants have so far failed to refer to any science. I never criticized your use either of the press release or the primary paper. I am, in fact, impressed by your willingness to actually engage the science. Rather, what I said in both cases is that your views lacked context. Despite how it may appear to you, neither the press release or the actual paper was intended to address the concerns you raise, concerns which are clearly intended to cast doubt upon aspects of the paradigm within which the work was done. In my opinion, you would be best served reading a scientist eminent in this field who has made it his business to supply that context. Carroll is the best such source I can recommend.
However, you’re a big boy and if you don’t want to take my advice, so be it. I’ll start another thread with the sea anemone references to facilitate further discussion.
Scott Hatfield:
You're making what you think is a good argument. I'll try to answer it, but the point about urging you to read Carroll is so you can place that argument in context. You are clearly attempting to read things into the primary literature that the authors themselves almost certainly did not intend.
No, I'm not trying to make my argument (as I don't really have one aside from expecting the proffered TENS explanation that has yet to materialize) so much as I'm endeavoring to drag your argument back to my specific question(s), which I won't bother repeating. And it's ok to not have an answer. "I don't know, perhaps someone else will" or "I'll find out" have always been perfectly good 'unincriminating' answers.
I've not read anything into the primary literature that wasn't already typed there by its authors. I linked and copied the points I've read from the article. I've repeatedly asked for how evolution explains that evidence (yes, I've argued when those answers were off-point or inapplicable). But that the authors didn't specifically address how TENS (etc.) explains their evidence is not to me suggestive of anything per se. I try to avoid arguments from silence (which is why I press for evidenciary confirmation of details), except when the silence follows from specific and repeated questions.
See, Carroll explains this stuff with far greater verve and wisdom than I can muster, and he places it in a broader context than the paper you’re trying to hang your hat on.
It is precisely that goal-post shift from the specifics of Nematostella vectensis to Carroll's broad generalizations (such as with "immortal genes") that sweeps the issue from view. Had the issue been the broad context Carroll popularizes, you might have a point. But the issue was and still remains how "modern evolution theory" explains the mechanisms by which Nematostella vectensis 'evolved' several hundred million years in advance unexpressed, highly conserved and orthologous, complex genes expressed in humans and other modern bilaterians. So far, it was not "immortal genes" nor natural selection (as these neither create new traits nor operate on existing unexpressed traits), nor seemingly chance contingency (as the unexpressed complexity and orthology with recent bilaterians is so high). When Carroll addresses the specifics raised earlier above (and repeated again below re., pg. 88) for example, then you'll have a point citing him.
So, instead of being offended that I refer you to a popularization, please consider the possibility that the line of reasoning you’re attempting to develop will need to be nested in that broader context in order to find a wider audience.
Not so much offended as that implies insult, which I don't perceive you as insulting, but I was irritated that in spite of my repeated requests for the hard scientific evidence, you proffered instead "immortal genes" (seemingly unaware of their inapplicability to unexpressed genes). And I'm not looking to find a wider audience. I'm fact-finding. I want to see the evidence whereby TENS (etc) explains how Nematostella evolved its particular genome.
To the best of my knowledge, no one is claiming that ‘unexpressed genes were conserved.’ If that’s your understanding, I think you’re misreading the data. If I’m wrong on that point, if someone in a peer-reviewed publication has actually suggested otherwise, I’d be delighted to look at that.
As previously cited:
(pg. 88) "Introns that are shared between Nematostella and vertebrates and/or other bilaterians are most parsimoniously interpreted as conserved ancient eumetazoan introns (40). Not only are the numbers of exons per gene similar between Nematostella and vertebrates, but the precise location and phase (i.e., the positioning of the splice sites relative to codon boundaries) of introns are also highly conserved between the anemone and human (Fig. 2A)."
‘The Making of the Fittest’ relies more heavily on the work of others, and it’s more user-friendly than the other book, but there’s plenty of evidence presented, with plenty of citations.
Ok, perhaps then I was misinformed. I will try to verify the presence of citations and get back. The book is not searchable on line (that I'm aware of). If you have a link to its bibliography and/or footnotes from the "immortal gene" chapter, that would be appreciated.
The title doesn’t refer to your honest attempts to engage the literature, but to the fact that Vox and his syncophants have so far failed to refer to any science. I never criticized your use either of the press release or the primary paper. I am, in fact, impressed by your willingness to actually engage the science.
Fair enough.
Scott Hatfield:
To the best of my knowledge, no one is claiming that ‘unexpressed genes were conserved.’ If that’s your understanding, I think you’re misreading the data. If I’m wrong on that point, if someone in a peer-reviewed publication has actually suggested otherwise, I’d be delighted to look at that.
As I reparse your question more carefully, I realize I have conflated "unexpressed gene" with unexpressed gene segment (intron).
The cite (repeated below) goes to conserved introns (never expressed) rather than complete genes which are expressed (the exon portion).
As previously cited:
(pg. 88) "Introns that are shared between Nematostella and vertebrates and/or other bilaterians are most parsimoniously interpreted as conserved ancient eumetazoan introns (40). Not only are the numbers of exons per gene similar between Nematostella and vertebrates, but the precise location and phase (i.e., the positioning of the splice sites relative to codon boundaries) of introns are also highly conserved between the anemone and human (Fig. 2A)."
I'm not sure if the nuance in your question (re conserved unexpressed genes as opposed to conserved unexpressed introns) was intentional or just unwittingly following my own mistaken conflation.
There is also this cite from the article:
(pp. 89-90) "The conserved linkage is extensive, and it accounts for a large fraction of the ancestral eumetazoan set. ... The 40 human segments that show conserved synteny with Nematostella cover half of the human genome. Within such human segments, typically 40 to 50% of eumetazoan-derived genes have counterparts in syntenic Nematostella segments, and vice versa. This is a notable total, given that any chromosomal fusions and subsequent gene order scrambling on either the human or Nematostella lineage during their ~700 million years of independent evolution would attenuate the signal for linkage."
Starwind, I thank you for taking the time to work through some of the nuances. I'm glad that we were able to weather a difficult moment (wherein some stuff was inadvertently conflated) without charges of 'bad faith.' You certainly deserve points for showing integrity with respect to Carroll and the conceptual problems.
I want to show good faith, then, and return to the matter I probably meant to address but failed to do so previously, namely your brief:
I want to see the evidence whereby TENS (etc) explains how Nematostella evolved its particular genome.
I want to be candid. First point: the 'modern synthesis' of the 1940's is not so modern any more, and the general rule in biology seems to be that 'there are always exceptions'. As our knowledge of molecular systematics has grown, we observe phenomena that strictly speaking are not part of the original modern synthesis, but which (once demonstrated) are pretty consistent with same, even predicable: things like endosymbiosis, gene duplications, large-scale chromosomal rearrangements, etc
The evo-devo people think that these processes can dramatically spur the emergence of organismal novelties, phenomena that are not well-described by natural selection alone. If we take 'TENS' as a gloss strictly for the old version of the modern synthesis, then I would have to affirm that TENS, on its' own, is unable to account for many of these details.
(gulp!) I hope no one 'quote-mines' me by leaving out the first part of the previous sentence. I think it's important to note that I view these other processes mentioned as supplementary to TENS, rather than contradictory.
But I think also a further confession is needed, and again I hope I don't get 'quote mined'. I don't think evolutionary biologists have enough data yet to place much confidence in any particular scenario of genomic evolution. The sea anemone genome promises to be an important model system because it will help provide more data to evaluate these claims. In fact, the findings of Putnam et al seem to provide evidence for one model of intron evolution over another. And that's a good thing, and another example of the sort of general prediction which, by being testable, leads to good science.
Scott Hatfield:
I don't think evolutionary biologists have enough data yet to place much confidence in any particular scenario of genomic evolution.
Agreed. Further, Darwinian natural selection does not account for all evolutionary genetic change. There is also the "Neutral Theory of Molecular Evolution" to consider. Here are the two founding primary papers:
Evolutionary rate at the molecular level (Kimura, 1968)
Non-Darwinian Evolution (King & Jukes, 1969)
As for you risking being 'quote mined', such would also reveal the intellectual dishonesty of those whose argument otherwise can't cope with scientific nuance and uncertainty. There remain extremists in all areas who are "often in error but never in doubt". It is they who do science and theology a disservice. Would that they could exercise more humility, rigor and accuracy, but then they'd have no argument.
I find absolutely nothing in your prior post that I would not affirm in the strongest terms. I actually have an essay project that I give as a summary assessment to my high school biology classes on evolution, and one of the possible topics they can pick (few do, for obvious reasons) is the 'neutral theory'.
Again, if 'TENS' is taken as being synonymous with the original 'modern synthesis', and only consistent with those things in the original formulation, it would be something like dogma and I wouldn't hesitate to reject it. The irony, of course, is that the scientific community holds no such position. Even ultra-Darwinians like Dr. Dawkins admit endosymbiosis, Kimura's work, etc.
The problem on my side of the aisle is to a large extent not the evident pluralism of causation (which is widely accepted) but rhetorical overkill on behalf of the one agency that is well-characterized (natural selection). Sometimes that rhetorical excess just reflects the relative confidence the writer affords natural selection in the scheme of things. I am sure I am not making any great admission, though, when I acknowledge that on occasion the motive is less innocent, representing the cooption of a pretty decent theory for a political and theological agenda.
Scott Hatfield:
‘The Making of the Fittest’ relies more heavily on the work of others, and it’s more user-friendly than the other book, but there’s plenty of evidence presented, with plenty of citations.
Ok, perhaps then I was misinformed. I will try to verify the presence of citations and get back.
Update:
So, I got to a bookstore today and did browse "The Making of the Fittest", mostly chapter 3 "Immortal Genes". As my 'informant' told me, there were no footnotes within the chapter, nor were any passages footnoted. Credits were given for the photographs. At the end of the book is an appendix with "further reading suggestions" organized by chapter with some very general hints as to what kind of topic dealt with in the chapter can be found discussed somewhere (but no specific references) within the suggested further reading material.
As I suspected, it is just a popularization with no citations given as to where to look to get the background supporting material on some factoid - certainly not like research papers where most factoids are footnoted and cited to aid in followup research.
The reader is forced to read all the suggested material in its entirety for at least the chapter, and then guess at what portions Carroll deemed pertinent to his writing.
Otherwise, the reader is forced to accept the author's opinions verbatim, there is no recouse to check on what his specific claims are based.
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