The problem with evo devo

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Last week, I gave a talk at UNLV titled "A counter-revolutionary history of evo devo", and I'm afraid I was a little bit heretical. I criticized my favorite discipline. I felt guilty the whole time, but I think it's a good idea to occasionally step back and think about where we're going and where we should be going. It's also part of some rethinking I've been doing lately about a more appropriate kind of research I could be doing at my institution, and what I want to be doing in the next ten years. And yes, I want to be doing evo devo, so even though I'm bringing up what I see as shortcomings I still see it as an important field.

I think of myself as primarily a developmental biologist, someone who focuses on processes in embryos and is most interested molecular mechanisms that generate form and physiology. But I'm also into evolution, obviously, and recently have been trying to educate myself on ecology. And this is where the conflicts arise. Historically, there has been a little disaffection between evolution and development, and we can trace it right back to Richard Goldschmidt and the neo-Darwinian synthesis.

There is minimal consideration of development in the synthesis. The big man in the interdisciplinary study of evolution and development at the time of the formulation of the synthesis was Goldschmidt, who actually raised some grand and important issues. He was interested in sex differences; the same genome can give rise to very different forms, male and female. He was interested in metamorphosis; the same genome produces both a caterpillar and an adult moth. And he was interested in phenocopies; the same genome can generate alternative forms under the influence of environmental factors. He had some very speculative ideas about global systemic mutations that haven't really panned out, and his ideas were tarred with the label "hopeful monsters", which didn't help either. It was non-Darwinian! It argued for abrupt transitions! I'll defer to Gould's defense of Goldschmidt, though, and would say that those weren't good reasons to reject some challenging ideas.

The charge that stung, though, was Ernst Mayr's accusation that Goldschmidt believed that new species could arise by a single fortuitous macromutation in a single individual, that Goldschmidt had abandoned or failed to grasp one of the most essential principles of evolutionary thought: that evolution occurs in populations, not individuals. He did not understand the concept of population thinking. I don't think he was entirely guilty of that, but I have to concede that there was a disjoint there: as a developmental biologist, Goldschmidt would wonder first and foremost about the kinds of genetic rearrangements that would generate an evolutionary novelty, and just assume that a superior morph would propagate through the population, a process of relatively little interest; while an evolutionary biologist would be less interested in the developmental details of the generation of the phenotype, and much more interested in the mechanics and probabilities of its spread through a population.

Evolutionary biologists and developmental biologists think differently, and that creates a conflict between the evo and the devo. I'm not unique in noting this: Rudy Raff included a table in his book, The Shape of Life, which I'll reproduce here, with a few modifications of my own.

QualityEvolutionary BiologistsDevelopmental Biologists
CausalitySelectionProximate mechanisms
GenesSource of variationDirectors of function
TargetTrans elements
(coding sequence)
Cis elements
(regulatory)
VariationDiversity & changeUniversality & constancy
HistoryPhylogenyCell lineage
Time Scale101-109 years10-1-10-7 years

Modified from Raff, 1996

Those different emphases can lead to biases in where we place the importance of various processes. I'll focus on just two: causality and variation.

When we're looking at the process of change within our domains, evolutionary biologists have already mastered the art of population thinking: everything is about propagation of patterns of variation within a population. There aren't explicit mechanisms that generate subtypes to fit the range of roles available. Instead, a cloud of forms is created by chance variation and the unfit are selected out. Developmental biologists, on the other hand, see an organism with a constellation of necessary and dedicated functions — there must be a nervous system to regulate behavior, there must be a gut to process food — and specific molecular mechanisms to programmatically generate them. Embryos do not proliferate a mass of cells with random variants, and then use the ones that secrete digestive enzymes for the gut and the ones that generate electrical impulses for the brain. A lot of development papers really do talk about nothing but proximate sequences of causal interactions that lead to a specific function or fate.

To an evolutionary biologist, variation is the stuff of interest: populations with no variation are not evolving (it's a good thing such populations don't exist, or if they do, chance will swiftly change the situation). To your average developmental biologist, variation is noise. It clutters the interpretation of the data. We want to say, "Here is the mechanism that produces this tissue type," not "Here is the mechanism that sometimes produces this tissue type, in some organisms, sometimes with other mechanisms X, Y, and Z." We generally love model systems because they allow us to establish an archetype and see a reliable pattern. In the best case, it gives us a solid foundation to work from; in the worst case, we forget altogether that there is more complexity in the natural world than is found in our labs. I would be the first to admit that laboratory zebrafish, for instance, are tremendously weird, inbred, specialized creatures…but they're still extraordinarily useful for getting clean results.

I will also be quick to admit that the above is a bit of a caricature. Of course many developmental biologists reach out beyond the simplistic reduction of everything to linear, proximate causes. Raff, in that book, goes on to discuss specifically all of the problems of model systems and how they distort our understanding of biology; I could cite researchers like David Kingsley who specifically study variation in natural populations; Ecological Developmental Biology, which describes the interactions between genes and environment; and of course there are all those scientists at marine stations who aren't staring at tanks full of inbred specimens, but are going out and collecting diverse forms in the wild. I am admitting a bias, but the best of us work hard to overcome it.

And then…we sometimes slip. I highly recommend Sean B. Carroll's Endless Forms Most Beautiful: The New Science of Evo Devo as an excellent introduction to evo devo, I even use it in my developmental biology course. In reducing the discipline to a popular science book, you can see what had to be jettisoned, though, and unfortunately, it's that whole business of population thinking and environmental influences (clearly, Carroll knows all that stuff, but in distilling evo devo down to the basics, that developmental bias is what emerges most clearly). Here, for instance, is the admittedly sound-bitey one sentence summary of what evo devo is from the book:

The Evo Devo Revolution

"The comparison of developmental genes between species became a new discipline at the interface of embryology and evolutionary biology--evolutionary developmental biology, or 'Evo Devo' for short."

Sean B. Carroll, 2005

Again, this is not a criticism of the book, which does what it does very well, that is, describe the mechanistic process of development and the regulatory logic behind it, but notice the missing words in that abbreviated description: populations and environments don't really come into play. All we've got there (and this is a bit unfair to Carroll) is comparisons of genes between species, which is enough to show common descent and relationships between the phyla, but it doesn't say how they got that way — which is an unfortunate deficiency for a discipline that is all about how things get that way!

That's what I'm concerned about. Right now, evo devo is far more devo than evo; we really need to absorb some more lessons from our colleagues in evolutionary biology. A more balanced evo devo would weight variation far more heavily, would be far more interested in diversity within and between populations, and would prioritize plasticity and environmental influences far more. If we did all that, it wouldn't be a revolution — because it would embrace everything that is already in evolution — but would be what Pigliucci calls the Extended Evolutionary Synthesis. What we'd have is a better appreciation of this well-known aphorism:

"Evolution is the control of development by ecology…"

Van Valen, 1973

That's the holy trinity of biology: evolution, ecology, development. Our goal ought to be to bring all three together in one beautiful balance.

triquetra.jpg

(Yeah, I stole the triquetra. We'll use it far more wisely than the religious.)

(Also on FtB)

53 Comments

This is food for much thought. I just wanted to mention that there have been, even before the evo-devo era, evolutionary biologists who considered developmental processes important in their thinking. For example:

* Gavin de Beer (Embryos and Ancestors, 1930)

* Julian Huxley (Problems of Relatuve Growth, 1935)

* Conrad H. Waddington (various papers and books)

and of course

* Stephen Jay Gould (Ontogeny and Phylogeny, 1977)

But of course, they did not have the developmental genes in hand, ones that have made evo-devo such a fascinating story.

This is analogous to studying complex patterns like the weather. It is very hard to get the big picture and see gross patterns when dealing only with snippets of scattered local weather.

About 20-some years ago, the National Weather Service laid off all of its meteorologists who were manning local weather stations all over the country. Now nearly all weather stations are robust, automated stations, and there are far more of them feeding their data into a central location along with all the satellite imaging.

The same story is going on in geophysics.

And the detectors at the Large Hadron Collider are huge arrays of detectors that handle and integrate far larger amounts of raw and partially processed date in order to pick up on patterns that can only emerge from huge amounts of data. This is because the phenomena that are being searched for are such a small percentage of the total number of other effects influencing the data.

This is a common feature of emergent phenomena. One cannot get the overall picture of an ant or bee colony by watching the activities of an individual ant or bee.

It is not surprising that looking only at things at the cellular level will not give a clear picture of evolution without also having that bigger picture involving populations. It seems that both are equally important.

I was under the impression that “new species…arise by a single fortuitous macromutation in a single individual…” and then that mutation spreads through the population - that’s the only way it can work. I am not a biologist, but that’s the way I remember learning it.

Paul Burnett said:

I was under the impression that “new species…arise by a single fortuitous macromutation in a single individual…” and then that mutation spreads through the population - that’s the only way it can work. I am not a biologist, but that’s the way I remember learning it.

It should be obvious that it *can’t* work that way. If a new species arose through a single mutation, and that new species were reproductively isolated from the old species (which is what speciation generally refers to), then the new mutation can’t spread through the population – the possessor of the mutation is (very temporary) a new species all by itself and doesn’t interbreed with the rest of the population. Speciation by mutation must arise gradually, through multiple mutations, no one of which causes reproductive isolation. There are mathematical models in which only two loci change, but one just won’t work.

The actual complete speciation would have to occur at a level that is chemically more tightly bound than the levels of actual development where the binding energies are much smaller (0.01 eV as compared to 1 eV).

This is true of all complex systems that are comprised of increasingly complex and increasingly more loosely bound systems built on top of a more robust “core” that provides an underlying template.

So it should not be surprising that changes in the frequencies of alleles affecting development would gradually isolate populations until “the big but rare event” that affected the “core” made interbreeding impossible.

Mike Elzinga said: ???

Are you trying to Sokal me?

John Harshman said:

Mike Elzinga said: ???

Are you trying to Sokal me?

:-)

Yeah, I’m reading that, shaking my head and reminding myself to stop multitasking when trying to write something coherent. I got phones going, repairs going, tracking down some information, and several projects on the computer going. Sheesh!

What I was attempting to say was that phenotypic characteristics in a population on which selection acts are not necessarily due to direct changes to the actual numbers of chromosomes (in animals, I believe. It’s different in plants as I understand it, sex is much more varied).

If this is true, then the binding energies of molecules involved in those phenotypic changes are much smaller than those in the genes themselves; something like a hundred times smaller.

So it must be the case that the phenotypic changes that result in the inability to interbreed and produce viable offspring have already taken place before actual changes in the DNA or chromosome length. I would think that a change in chromosome length, for example, requires more energy to break or rearrange bonds than for many other bonds involved in phenotype. Such a change is not only less probable, it would produce an individual incapable of breeding with the other members of the population.

(Man, in the time I tried to write that, I had to drop everything and try to diagnose an electrical problem over the phone. And now I have to take out the trash.)

This comment has been moved to The Bathroom Wall by Joe Felsenstein (assuming PZ doesn’t have time to moderate this thread) because Byers is never interested in really discussing science.

Speaking of trash…

Paul Burnett said:

I was under the impression that “new species…arise by a single fortuitous macromutation in a single individual…” and then that mutation spreads through the population - that’s the only way it can work. I am not a biologist, but that’s the way I remember learning it.

In populations where sexual reproduction/meiosis is required for long term reproduction, a new mutation that affected the phenotype in so extreme a way as to reproductively isolate the individual it arose in would not be passed on, for obvious reasons.

(Some such species may have a life cycle in which mitotically reproducing forms play a role, but if some form of sexual reproduction is necessary for the long term future of the species, what you describe is impossible. Please note that in vitro fertilization and so on are still methods of sexual reproduction.)

In organisms that reproduce mainly by mitosis, which are a vast proportion of the biosphere, we use nomenclature derived from the study of animals and plants purely for historical reasons and convenience, e.g. http://en.wikipedia.org/wiki/Bacterial_taxonomy. In the case of these organisms, no sex partner is required for reproduction. Capacity for lateral gene transfer may be required for individual viability, but that doesn’t require the same level of specificity that sexual reproduction. Such populations evolve via the same major mechanisms as other populations - genetic variability, natural selection, genetic drift, etc. However, the concept of “species” is quite different than it is for sexually reproducing organisms.

Developmental biology focuses on the development of multicellular organisms with more than one type of differentiated somatic cells. For the most part, the models studied in developmental biology are sexually reproducing organisms, (C. elegans has an interesting system but it’s still sexual).

Mike Elzinga said:

John Harshman said:

Mike Elzinga said: ???

Are you trying to Sokal me?

:-)

Yeah, I’m reading that, shaking my head and reminding myself to stop multitasking when trying to write something coherent. I got phones going, repairs going, tracking down some information, and several projects on the computer going. Sheesh!

What I was attempting to say was that phenotypic characteristics in a population on which selection acts are not necessarily due to direct changes to the actual numbers of chromosomes (in animals, I believe. It’s different in plants as I understand it, sex is much more varied).

If this is true, then the binding energies of molecules involved in those phenotypic changes are much smaller than those in the genes themselves; something like a hundred times smaller.

So it must be the case that the phenotypic changes that result in the inability to interbreed and produce viable offspring have already taken place before actual changes in the DNA or chromosome length. I would think that a change in chromosome length, for example, requires more energy to break or rearrange bonds than for many other bonds involved in phenotype. Such a change is not only less probable, it would produce an individual incapable of breeding with the other members of the population.

(Man, in the time I tried to write that, I had to drop everything and try to diagnose an electrical problem over the phone. And now I have to take out the trash.)

Sorry, but as far as I can tell you still are making zero sense. No changes in chromosome number, or even length, were mentioned or implied by anyone here. Binding energies are, as far as I can see, irrelevant. Your post appears to have nothing at all to do with biology, and you seem to be under several false impressions about evolution whose natures are unfortunately not completely clear. Perhaps you should wait until you have more time to think this out before posting.

John Harshman said:

Sorry, but as far as I can tell you still are making zero sense. No changes in chromosome number, or even length, were mentioned or implied by anyone here. Binding energies are, as far as I can see, irrelevant. Your post appears to have nothing at all to do with biology, and you seem to be under several false impressions about evolution whose natures are unfortunately not completely clear. Perhaps you should wait until you have more time to think this out before posting.

Binding energies irrelevant? Are you freaking out of your mind, John?

John Harshman -

I think when Mike says -

What I was attempting to say was that phenotypic characteristics in a population on which selection acts are not necessarily due to direct changes to the actual numbers of chromosomes (in animals, I believe. It’s different in plants as I understand it, sex is much more varied).

He is assuming that in the phrase “new species…arise by a single fortuitous macromutation in a single individual…”, “single fortuitous macromutation” refers to a change in karyotype.

If my interpretation here is correct I will note -

1) Changes in chromosome number/morphology may or may not be related to significant changes in DNA sequence that could be said to relevantly alter the genome. For an extreme example, not related to speciation but of interest as an example, the type of abnormal chromosome translocations associated with some types of cancer is very much a major type of somatic mutation, often leading to transposition of a constituitively expressed gene (for a given cell type) with a gene whose expression is normally restricted, so that the latter, or some highly abnormal fusion protein that includes an active domain of the selectively expressed protein, is overexpressed and has dramatic effects on the cell.

However, things like chromosome fusion can occur, without disruption to any genes or their ability to be correctly expressed.

2) A mutation that reproductively isolated an individual would not need to have any effect on chromosome number or morphology, and a chromosome number change may not totally isolate an individual.

3) It is true that karyotype differences do seem to be associated with speciation, and that species tend to be said to have their own distinct chromosome number. It does seem likely that chromosome number/morphology changes may have something to do with speciation in eukaryotes. http://en.wikipedia.org/wiki/Chromo[…]us_organisms

On the other hand, there are some breeding populations in which some individuals have slightly different karyotypes than other individuals, yet viable offspring can result.

However, the same principle of “it takes at least two to tango” applies. Otherwise healthy humans may be infertile if they have a karyotype that does not impede normal gene expression for development and viability, but that is not reproductively compatible with the karyotype of available partners (combined karyotype of gametes will be missing large amounts and necessary genetic material and triploid for other genetic material).

http://en.wikipedia.org/wiki/Robert[…]ranslocation

If this is true, then the binding energies of molecules involved in those phenotypic changes are much smaller than those in the genes themselves; something like a hundred times smaller.

I’m not 100% sure what Mike means here, either.

harold said:

John Harshman -

I think when Mike says -

What I was attempting to say was that phenotypic characteristics in a population on which selection acts are not necessarily due to direct changes to the actual numbers of chromosomes (in animals, I believe. It’s different in plants as I understand it, sex is much more varied).

He is assuming that in the phrase “new species…arise by a single fortuitous macromutation in a single individual…”, “single fortuitous macromutation” refers to a change in karyotype.

If my interpretation here is correct I will note -

1) Changes in chromosome number/morphology may or may not be related to significant changes in DNA sequence that could be said to relevantly alter the genome. For an extreme example, not related to speciation but of interest as an example, the type of abnormal chromosome translocations associated with some types of cancer is very much a major type of somatic mutation, often leading to transposition of a constituitively expressed gene (for a given cell type) with a gene whose expression is normally restricted, so that the latter, or some highly abnormal fusion protein that includes an active domain of the selectively expressed protein, is overexpressed and has dramatic effects on the cell.

However, things like chromosome fusion can occur, without disruption to any genes or their ability to be correctly expressed.

2) A mutation that reproductively isolated an individual would not need to have any effect on chromosome number or morphology, and a chromosome number change may not totally isolate an individual.

3) It is true that karyotype differences do seem to be associated with speciation, and that species tend to be said to have their own distinct chromosome number. It does seem likely that chromosome number/morphology changes may have something to do with speciation in eukaryotes. http://en.wikipedia.org/wiki/Chromo[…]us_organisms

On the other hand, there are some breeding populations in which some individuals have slightly different karyotypes than other individuals, yet viable offspring can result.

However, the same principle of “it takes at least two to tango” applies. Otherwise healthy humans may be infertile if they have a karyotype that does not impede normal gene expression for development and viability, but that is not reproductively compatible with the karyotype of available partners (combined karyotype of gametes will be missing large amounts and necessary genetic material and triploid for other genetic material).

http://en.wikipedia.org/wiki/Robert[…]ranslocation

If this is true, then the binding energies of molecules involved in those phenotypic changes are much smaller than those in the genes themselves; something like a hundred times smaller.

I’m not 100% sure what Mike means here, either.

Binding energies are exceedingly relevant, but in this context, the binding energies associated with a mutation that causes reproductive isolation might not be much different from those associated with a chemically similar mutation, that does not.

However, I’ll wait for Mike to clear this part up.

harold said:

Binding energies are exceedingly relevant, but in this context, the binding energies associated with a mutation that causes reproductive isolation might not be much different from those associated with a chemically similar mutation, that does not.

However, I’ll wait for Mike to clear this part up.

I was having a rather hectic day yesterday. I produced a muddle.

Harold hits closer to what I was trying to get at. However, let me restart by posing my thoughts as a question.

As compared to the parent population, what does the genetic profile of a species in transition look like? Where are the differences occurring and where will genetically isolated speciation occur?

At the biochemical level, what makes the difference between a species that is not just isolated geographically or by morphology, but chemically?

I presume the DNA is sufficiently different that interbreeding, even if attempted by artificial insemination, would not produce viable offspring.

Does completed genetic isolation take place before changes in the more tightly bound molecules that form the fundamental template for the species, or does some fundamental change have to take place in a molecule that is the most tightly bound in the genetic profile?

The reason I refer to the most tightly bound molecules in the template of the species is because that is the part of the template that has the least probability of changing and will thus be expected to persist the longest.

I don’t know the answer myself, I was attempting to speculate using some analogies from chemistry and physics; and I was trying to do it in the midst of chaos yesterday.

This relates to the issue of a mutation in a single individual that renders it a new species genetically, but since that individual is unlikely to be able to breed with other offspring of the parent population, there is little likelihood that this (hopeful monster) can be the beginning of the daughter species.

I can conceive of ways around this, but that led me to the speculations about where in the changing genetic profile interbreeding becomes impossible.

As compared to the parent population, what does the genetic profile of a species in transition look like? Where are the differences occurring and where will genetically isolated speciation occur?

At the biochemical level, what makes the difference between a species that is not just isolated geographically or by morphology, but chemically?

I presume the DNA is sufficiently different that interbreeding, even if attempted by artificial insemination, would not produce viable offspring.

1) Any two populations whose genomes cannot be combined, even by artificial insemination, to produce viable offspring, would certainly be different species, by any reasonable standard.

In fact, the term species is an operational one, usually referring to human-observable distinct populations that tend not to reproduce with one another. Some closely related species can hybridize to produce viable and fertile offspring, but tend not to. The offspring of such matches may tend to be less fertile than non-hybrids, and may tend to lack highly adaptive innate behaviors. E.g. Ligers and Tiglons are not very fertile (but not completely infertile). Tigers and lions have quite different behaviors and tend to favor different environments, and in the wild, a “hybrid” behavior pattern might not be as adaptive in any environment as the more specialized behaviors.

In general, reproductive isolation probably occurs gradually. Here is a decent treatment of one type of speciation. http://en.wikipedia.org/wiki/Sympatric_speciation

Does completed genetic isolation take place before changes in the more tightly bound molecules that form the fundamental template for the species, or does some fundamental change have to take place in a molecule that is the most tightly bound in the genetic profile?

The reason I refer to the most tightly bound molecules in the template of the species is because that is the part of the template that has the least probability of changing and will thus be expected to persist the longest.

I don’t know what you mean by “fundamental template for the species”. That borders on sounding like something from Plato’s World of the Forms.

The nucleic acid genome of an organism, and let’s leave viruses aside so that we can say “DNA genome” and not worry about whether viruses are organisms, is sometimes semi-accurately described as the template for an organism, in what is a reasonable simplification. In fact, the genome of a zygote is never naked, and the cytoplasm of the zygote itself already contains proteins, RNA, etc. Development cannot take place without an appropriate environment, including the original zygote environment for the nuclear (and other, such as mitochondrial) genome, itself in an appropriate environment, such as an appropriate part of a uterus. Phenotypes, including behavior, are strongly modified by environmental experience in many organisms. Having said that, the sequence of a genome could, hypothetically, tell us what kind of organism the genome was from, whether it contained mutations incompatible with development to fertile adult, perhaps what limits adult phenotype might fall between if reached, etc. In theory, knowing the sequence of someone’s genome would not tell you whether the genome was a product of an early miscarriage or carried to term, whether the person would be exposed to toxins or infections in utero, whether they would die of an infection at an early age (it might give some clues to relative vulnerability to some infections), whether they could read, what language they would speak, whether they had been disabled in a random accident, etc, etc. However, it would tell you whether it was a human genome, whether any known major genetic disorder was present, and a number of other things.

This relates to the issue of a mutation in a single individual that renders it a new species genetically, but since that individual is unlikely to be able to breed with other offspring of the parent population, there is little likelihood that this (hopeful monster) can be the beginning of the daughter species.

A reproductively isolated individual is nearly always best thought of as an infertile member of the species they were born into, not as a “species of one”.

I can conceive of ways around this, but that led me to the speculations about where in the changing genetic profile interbreeding becomes impossible.

Not known, and there may be no hard, fast rules.

However, it’s easy to do a crude model. Suppose there is a population with three genes, and one allele at each gene, A, B, and C respectively. They’re all ABC homozygotes. No genders in this crude example, but sexual reproduction - offspring get one allele from each parent.

One individual with a mutation is born and is a heterozygote, ABC/ABD. No problem breeding. Eventually some ABD/ABD homozygotes exist.

For whatever reason, the D allele causes those who possess it to prefer to reproduce with each other, so ABD/ABD homozygotes become common. There is behavioral isolation, but any allele combination is consistent with full fertility.

A new mutation arises again, so that some individuals are ABD/ABE. Allele E creates a strong selective advantage, unless allele C is also present, in which case it is fatal.

There will be no ABE/ABC individuals. ABC/ABC and ABE/ABE are genetically isolated from each other. There may be a tendency for two subpopulations to form, one mainly ABC/ABC, and one mainly ABE/ABE. There will still be individuals with one or two D alleles, so genes will still potentially be exchanged between these populations, but at a slowing rate. And so on. This is basically a very crude but not worthless modeling of sympatric speciation, where barriers between subpopulations are genetic/behavioral. In allopatric speciation, a geographic barrier separates a formerly unified population.

What you have to remember is that a mutation does not *cause* speciation. Mutations arise within a population, over time, and dependent on the number of members of the population. Their individual frequency within the population will be accordingly very low. However, when a very small subset of a population is reproductively isolated, and by very small this maybe a breeding pair, or pregnant mother, and mutation in that small population suddenly finds itself at a high frequency, independently of selection. If that small subset then breeds amongst itself, that mutation can quickly become fixed due only to genetic drift, though selection may assist. Selection will determine whether the population survives. If the population survives through about fifty or so generations, these fixed mutations (it inherited from the parent population) will distinguish it from the parent population where they are at very low frequency or may have been even eliminated due to genetic drift. By then the new species is populous enough to acquire and retain new mutations. These new mutations are low frequency in the new species, and will stay so while the population is large, and be constantly subject to elimination by drift.

This is the why speciation is in the realm of population genetics. How specifically a mutation leads to a particular feature, or what the members of the new species may look like compared to the parent population, that would seem to be the realm of evo-devo.

harold said:

I don’t know what you mean by “fundamental template for the species”. That borders on sounding like something from Plato’s World of the Forms.

Plato’s Forms are not necessary. Throughout most of complex systems of molecules that are growing on the back of a molecule that sets an underlying pattern, those subsequent stages in the hierarchy are normally constrained by the underlying pattern until that underlying pattern is so many levels of complexity deep down that the overlying patterns become the basis for subsequent developments.

Perhaps the complexities of molecules in living organisms are reaching levels where some underlying template provided by the DNA - or whatever is the lowest level robust molecule passing on “instructions” – has been long buried in higher level complexities.

I can imagine that there are huge differences from species to species; especially the more complex species. I would think however, that getting down to the level of viruses and bacteria, we would continue to see the underlying “template” or pattern even though there are large differences in the viruses and bacteria.

But there isn’t sex involved either. Sex is complicated.

Not known, and there may be no hard, fast rules.

However, it’s easy to do a crude model. Suppose there is a population with three genes, and one allele at each gene, A, B, and C respectively. They’re all ABC homozygotes. No genders in this crude example, but sexual reproduction - offspring get one allele from each parent.

One individual with a mutation is born and is a heterozygote, ABC/ABD. No problem breeding. Eventually some ABD/ABD homozygotes exist.

For whatever reason, the D allele causes those who possess it to prefer to reproduce with each other, so ABD/ABD homozygotes become common. There is behavioral isolation, but any allele combination is consistent with full fertility.

A new mutation arises again, so that some individuals are ABD/ABE. Allele E creates a strong selective advantage, unless allele C is also present, in which case it is fatal. There will be no ABE/ABC individuals. ABC/ABC and ABE/ABE are genetically isolated from each other. There may be a tendency for two subpopulations to form, one mainly ABC/ABC, and one mainly ABE/ABE. There will still be individuals with one or two D alleles, so genes will still potentially be exchanged between these populations, but at a slowing rate. And so on. This is basically a very crude but not worthless modeling of sympatric speciation, where barriers between subpopulations are genetic/behavioral. In allopatric speciation, a geographic barrier separates a formerly unified population.

Yes, that is what I had in mind, but you described it much better than I could have.

co:

Binding energies irrelevant? Are you freaking out of your mind, John?

Not to my knowledge. But I would be happy to have you explain why the binding energies of any particular molecules have relevance to speciation.

Mike Elzinga:

As compared to the parent population, what does the genetic profile of a species in transition look like? Where are the differences occurring and where will genetically isolated speciation occur?

I don’t know what a genetic profile is. In any population, there’s genetic variation. Some of it lies in differences of base at individual sites, i.e. a G instead of an A at some spot. Some of it is length differences, in which some individuals have a bit of sequence that others don’t. Some of these differences are selectively favored. If two populations of a species are geographically isolated and are under different selective regimes (or even if they aren’t, by chance), different alleles may become fixed in the populations. Sometimes an accumulation of several differences make interbreeding unlikely, either because individuals fail to consider each other as possible mates or because differences interfere with development. Did that answer your question? I will confess I’m not sure I know what you’re asking. At any rate, none of this is best understood at the level of chemical reactions, which is where you seem to be.

Does completed genetic isolation take place before changes in the more tightly bound molecules that form the fundamental template for the species, or does some fundamental change have to take place in a molecule that is the most tightly bound in the genetic profile?

Nobody knows what you mean by “tightly bound molecules” or “fundamental template”. These are not concepts useful in speciation genetics. But no fundamental changes have to happen. Gradual fixation in two populations of a set of mutually incompatible allele combinations will produce post-mating isolation. To exaggerate, if half your genome wants you to be a frog and the other half wants you to be a prince, you can see that there might be some problems arising during development. This isn’t chemistry, unless you count the chemistry of conflicting developmental signals, and that really isn’t a relevant way to think of it.

Consider a very simple model: two genes, A and B, with alleles a and a’, b and b’. The species begins with all individuals having an aabb genotype. No problem. Then the species range is cut in half by a wall (or whatever), dividing it into two populations X and Y, initially identical. Mutation a’ arises in X, and is for some reason advantageous, and so eventually becomes fixed. All X are now a’a’bb. Later, mutation b’ arises in X and is also advantageous, and also becomes fixed. No problem, since b is compatible with a’ and a’ is compatible with b’. However, it turns out that a is not compatible with b’; if both alleles are present, the embryo dies early in development. So if we take the wall away and allow population X (now a’a’b’b’) to mate with population Y (still aabb), we get an a’ab’b genotype, which is inviable. There you go, complete reproductive isolation with two mutations.

Chromosomal mutations are another matter. Some will produce reproductive isolation, some won’t. But none are required for speciation.

John Harshman said:

Not to my knowledge. But I would be happy to have you explain why the binding energies of any particular molecules have relevance to speciation.

It has to do with how susceptible a molecule is to change. A more tightly bound molecule requires larger perturbations from its environment to break it or rearrange it; so it persists longer.

If it also is a determiner of an underlying pattern that persists between species (e.g., Harold mentioned the “big cats” lions and tigers), then presumably molecules that are less tightly bound are involve in speciation, and it is only after more improbable events occur that lead to the rearrangement of that more tightly bound molecule that complete genetic isolation occurs.

I can explain things in physics, but I have a little more trouble with the terminology in biology. Many of us physicists hate to admit it, but we are a bit intimidated by biology.

Mike Elzinga said:

John Harshman said:

Not to my knowledge. But I would be happy to have you explain why the binding energies of any particular molecules have relevance to speciation.

It has to do with how susceptible a molecule is to change. A more tightly bound molecule requires larger perturbations from its environment to break it or rearrange it; so it persists longer.

If it also is a determiner of an underlying pattern that persists between species (e.g., Harold mentioned the “big cats” lions and tigers), then presumably molecules that are less tightly bound are involve in speciation, and it is only after more improbable events occur that lead to the rearrangement of that more tightly bound molecule that complete genetic isolation occurs.

I can explain things in physics, but I have a little more trouble with the terminology in biology. Many of us physicists hate to admit it, but we are a bit intimidated by biology.

Unless you are using this “more tightly bound” thing as a metaphor only, it really has nothing to do with genetics or speciation. The tightness of bonds has nothing to do with mutation. (Supercoiling of DNA does, a bit, but that isn’t what you’re talking about.) Now, if it’s a metaphor, I’m not clear on what it’s a metaphor for. Perhaps you could explain this in biological terms? There is no variable involved in the probability of mutation that I would analogize to “more tightly bound”.

Now in order to discuss the mechanics of mutation, there are a few basics to understand. Do you know the structure of DNA? Do you know what a point mutation is? Do you know what an indel is?

Mike Elzinga said:

John Harshman said:

Not to my knowledge. But I would be happy to have you explain why the binding energies of any particular molecules have relevance to speciation.

It has to do with how susceptible a molecule is to change. A more tightly bound molecule requires larger perturbations from its environment to break it or rearrange it; so it persists longer.

If it also is a determiner of an underlying pattern that persists between species (e.g., Harold mentioned the “big cats” lions and tigers), then presumably molecules that are less tightly bound are involve in speciation, and it is only after more improbable events occur that lead to the rearrangement of that more tightly bound molecule that complete genetic isolation occurs.

I can explain things in physics, but I have a little more trouble with the terminology in biology. Many of us physicists hate to admit it, but we are a bit intimidated by biology.

Mike -

John Harshman is talking from a population genetics perspective.

I love population genetics, but my applied biomedical education has more to do with molecular and cellular biology.

Molecular biology and population genetics are complementary. Molecular biology explains what happens more or less at the level of nucleotide molecules, and population genetics models how changes that result from molecular events spread through populations.

Molecular biology is a way of studying the biochemistry of a specific group of molecules.

Biochemistry is chemistry.

But here’s the thing, Mike.

As you yourself have pointed out, from a physicists perspective, terrestrial life proceeds within a boringly narrow range of energies.

Yes, lions and tigers are cats. They are similar to some recent common ancestor that they share. And all canines and cats have a common ancestor. And all placental mammals have a common ancestor. And all mammals have a common ancestor. And all vertebrates have a common ancestor. And so on.

But the chemistries of individual mutations are pretty similar. The reaction kinetics are pretty similar. Some parts of the genome experience some types of mutations more frequently than other parts of the genome. However, genes that are fundamental to morphological development are pretty much just as vulnerable to mutation as any others. When mutations occur in such genes, there is often an early termination of pregnancy, or sometimes an individual born that cannot survive long. The genome is a string of nucleotides bound up in supporting molecules, and divided into segments known as chromosomes.

What you seem to be conjecturing is that genes that are fundamental to basic development are less likely to experience mutation. Well, not that I know of. Although that in itself is not an unreasonable conjecture by any means. What I know of mutations and DNA repair mechanisms does not strongly suggest that to me, but certainly some kind of system that prioritizes repair of fundamental development genes in germ cells could hypothetically be selected for. As could nucleotide sequences that are stochastically a bit less susceptible to mutation. Or some such combination. But it would still be nucleic acid and protein biochemistry. And even if this were the case, it would probably apply more to the kinds of genes that lions and tigers share with fruit flies.

Speciation, though, can be adequately modeled as occurring due to hierarchical sequences of equally probable events. There is no current reason to conjecture that it necessarily involves some set of mutations that are less frequent than other types of mutations.

I can explain things in physics, but I have a little more trouble with the terminology in biology. Many of us physicists hate to admit it, but we are a bit intimidated by biology.

I wasn’t aware of this until the last few years. But I now realize what happens.

Despite my relative ignorance of science outside my areas of study, a biology degree requires at least some physics, math, chemistry, and computer science. More is common. I have some extra training in probability/statistics and took a physical chemistry course that wasn’t required. Many people do much more cross training. Basic stuff comes up. My celluar neurobiology course was a pretty good review of some basic electricity concepts.

Plenty of people seriously combine physical sciences with biomedical sciences, but when they do, they’re perceived as joining the biomedical community. What do you call a physicist who also takes a lot of biology courses? Typically, a biophysicist.

Anyone with the talent and work ethic to get a physics education has the ability to learn all the biology they ever want to know, and some of the greatest biologists came out of physics, but there is a lot of stuff in biology, and while the math we use is mainly (but not exclusively) stuff that was invented by 1800, there can be a lot of rather brilliant logic (not referring to anything I have done personally) and stochastic reasoning going on.

John Harshman said:

Unless you are using this “more tightly bound” thing as a metaphor only, it really has nothing to do with genetics or speciation. The tightness of bonds has nothing to do with mutation. (Supercoiling of DNA does, a bit, but that isn’t what you’re talking about.) Now, if it’s a metaphor, I’m not clear on what it’s a metaphor for. Perhaps you could explain this in biological terms? There is no variable involved in the probability of mutation that I would analogize to “more tightly bound”.

It’s not a metaphor. Any molecule, including the DNA helix, will have binding energies associated with various sites along the helix. Binding energies refer to the energy required to break a chemical bond or any other type of bond between molecules.

Back when DNA structure was deciphered using x-ray crystallography, the preparation of the samples involved pulling them out into an uncoiled length so that the x-ray diffraction pattern could be made clear and uncluttered by the folding. All molecules involve bonds and their binding energies; that’s chemistry and physics. DNA turned out to be what is sometimes referred to as a quasi-crystal. It has a well-defined arrangement that produces an x-ray diffraction pattern. It can be broken, unzipped, rearranged. All that involves binding energies.

Electrophoresis involves applying an electric field to a complex molecule and watching the parts drift apart in a gel according to binding energies and mass.

I can understand why biologists describing speciation would not necessarily use terms like binding energies. They are working with “blocks” or “units,” and their rearrangements, without necessarily asking what energies are actually involved in these rearrangements.

Biochemists and biophysicists will be thinking about binding energies as well as other energies involved in the operations of cells and other complex molecules and systems.

So, yes, binding energies are very much a part of speciation. Biology is chemistry and physics on a very complex scale.

harold said:

But the chemistries of individual mutations are pretty similar. The reaction kinetics are pretty similar. Some parts of the genome experience some types of mutations more frequently than other parts of the genome. However, genes that are fundamental to morphological development are pretty much just as vulnerable to mutation as any others. When mutations occur in such genes, there is often an early termination of pregnancy, or sometimes an individual born that cannot survive long. The genome is a string of nucleotides bound up in supporting molecules, and divided into segments known as chromosomes.

What you seem to be conjecturing is that genes that are fundamental to basic development are less likely to experience mutation. Well, not that I know of. Although that in itself is not an unreasonable conjecture by any means. What I know of mutations and DNA repair mechanisms does not strongly suggest that to me, but certainly some kind of system that prioritizes repair of fundamental development genes in germ cells could hypothetically be selected for. As could nucleotide sequences that are stochastically a bit less susceptible to mutation. Or some such combination. But it would still be nucleic acid and protein biochemistry. And even if this were the case, it would probably apply more to the kinds of genes that lions and tigers share with fruit flies.

You understood my question; that was what I was interested in. It appears that lots of types of bonds and bond energies are involved, and in any given organism, there isn’t any particular likelihood that weaker types of bonds are more likely to be involved in speciation than stronger ones.

I may not know the details, but that’s an important piece of information.

Interesting discussion. Noting Mike’s fondness for the emergent properties of systems of ever-increasing complexity, I had interpreted Mike’s comment about binding energies to, in this context, suggest DNA, as a higher “order” or an assembly of nucleotides, and “genes” as assemblies of DNA (roughly speaking). Further, that each “higher” level of complexity has a “higher” level of binding energy. Not that the actual energy levels are “higher” (in a strictly electrical sense), but just that there are (or need to be) more of them.

More specifically, it takes a certain amount of energy to create a single-point mutation. It takes (in general) multiple mutations over time to create heritable yet species-breaking changes, hence “more energy” for creating that new species. The larger the change, the “more energy” required over time.

(Noting from the above discussion that, while morphologically dramatic changes are certainly possible with the right single-point mutations, such changes are not likely to be heritable (even if survivable) and so are not likely to be effective at creating new species. Thus, successful species-breaking changes have a constrained “trajectory”, requiring “more energy” over time to succeed.)

I realize that’s all rather fuzzy and probably doesn’t comport well with the actual physics, chemistry, or biology, but it helped provide me with a conceptual framework for at least a little while. :-)

I simply don’t see Elzinga’s point. The energies required to generate errors are going to be trivial relative to the energetic costs of replication and meiosis.

I can understand why biologists describing speciation would not necessarily use terms like binding energies. They are working with “blocks” or “units,” and their rearrangements, without necessarily asking what energies are actually involved in these rearrangements.

This should not be taken to imply that biologists have never studied the chemical properties of DNA. There is abundant literature on the physical chemistry of nucleic acids and related topics. Much of it dates back many decades. It is often touched on in introductory biochemistry courses. There is, however, no need to reinvent this wheel. There is no lack of awareness of the kinetics of biochemical reactions. This simply isn’t what is emphasized in the study of molecular biology, genomics, or population genetics. However, the former two are built on the foundation of biochemical studies. Population genetics precedes molecular genetics but complements and is confirmed by molecular genetic data.

Mike Elzinga said:

It’s not a metaphor. Any molecule, including the DNA helix, will have binding energies associated with various sites along the helix. Binding energies refer to the energy required to break a chemical bond or any other type of bond between molecules.

While this is true, it has exactly nothing to do with the subject we’re talking about. First of all, mutation doesn’t involve the breaking of chemical bonds. Most mutations happen during replication. All it means is that the polymerase happens to incorporate the wrong nucleotide. OK, bond energies matter there. The probability of error depends on how long the incorrect base stays in position. Correct bases form hydrogen bonds with the template. Incorrect bases form hydrogen bonds too, but not very strong ones. But some are stronger than others, and so it’s much more likely for a G to be substituted for an A than for a C to be substituted.

Even so, this still has nothing to do with what we’re talking about.

Back when DNA structure was deciphered using x-ray crystallography, the preparation of the samples involved pulling them out into an uncoiled length so that the x-ray diffraction pattern could be made clear and uncluttered by the folding. All molecules involve bonds and their binding energies; that’s chemistry and physics. DNA turned out to be what is sometimes referred to as a quasi-crystal. It has a well-defined arrangement that produces an x-ray diffraction pattern. It can be broken, unzipped, rearranged. All that involves binding energies.

Again, true. But nothing whatsoever to do with speciation. And very little to do with mutation. We can perhaps agree that a biochemical study of various mechanisms of mutation would be useful. But even that doesn’t percolate up to the level of interest. Mutation can be adequately characterized without an understanding of any of this, and in fact thinking about it just gets in the way.

Electrophoresis involves applying an electric field to a complex molecule and watching the parts drift apart in a gel according to binding energies and mass.

I can understand why biologists describing speciation would not necessarily use terms like binding energies. They are working with “blocks” or “units,” and their rearrangements, without necessarily asking what energies are actually involved in these rearrangements.

The binding energies have nothing to do with the rearrangements.

Biochemists and biophysicists will be thinking about binding energies as well as other energies involved in the operations of cells and other complex molecules and systems.

As they quite properly should. So, yes, binding energies are very much a part of speciation. Biology is chemistry and physics on a very complex scale.

To the extent that everything can be described by quantum mechanical interactions, perhaps. But thinking about it this way is absolutely useless in discussing speciation, and almost useless in discussing mutation. Witness the fact that nothing you have said from this physical standpoint bears any resemblance to anything that happens in speciation. At bottom it may all be QM. But you are not just failing to see the forest for the trees. You are failing to see the forest for the atoms of which the trees are composed.

You understood my question; that was what I was interested in. It appears that lots of types of bonds and bond energies are involved, and in any given organism, there isn’t any particular likelihood that weaker types of bonds are more likely to be involved in speciation than stronger ones.

Actually, I don’t think this is true. There are a very few types of bonds and bond energies involved in mutation. Essentially, the hydrogen bonds between nucleotides on opposite strands. Adjacent bases on the same strand affect these energies slightly. I doubt that has any effect on mutations, unless it has something to do with the mutability of CpG doublets. Which I don’t know. Bonds typically are not broken during point mutation, as it generally happens during replication. Indels can result from broken strands, in which case the covalent phosphodiester bond is relevant. But as far as I know, all such bonds are identical. DNA undergoes various forms of supercoiling, but mutations generally happen when the DNA is uncoiled. Really, I don’t see anything for you.

This is reminding my about why I went into physics; physics is for the simple minded, and biologist are intimidating. ;-)

Bond breaking has to have something to do with mutations otherwise inducing mutations by exposing organisms with x-rays or gamma rays would not affect mutation rates. When replication occurs in the presence of broken bonds, errors begin to accumulate.

This is pretty basic in physics; and it is how we often do delicate preparation of samples for various kinds of study.

Harold mentioned “DNA repair mechanisms,” and this is some of the language that makes it very hard to talk across disciplines.

Those who have worked in condensed matter physics or materials science are well aware of the process of annealing. We do this with complex systems all the time. Defects and dislocations can be “self-repaired” or “healed” by bringing the system up to a temperature that allows the increased kinetic energies of atoms or molecules to move back into more stable positions (deeper wells).

I’ve mentioned things like hypothermia and hypothermia a number of times on other threads. Temperature changes have dramatic effects not only on metabolic processes but on mutations and on the sex of a developing embryo in some species. The rate at which crickets chirp, rates of development are all affected by temperature.

I have watched videos of the flow of cells in developing organs that are stark reminders of how physicists play around with the growth of materials by various means.

Many of the descriptions of all the “factories” inside of cells are ripe for abuse; and certainly ID/creationists have abused them. But these descriptions have a teleological quality to them that make a physicist nervous. We make similar things on a less complex scale, but we know what forces and interactions or gradients we are using to describe them.

I’m regretting having unintentionally dragged this thread off topic.

I’ll shut up now and go back to thinking.

Mike -

One more comment, because I think you’re almost there.

Bond breaking has to have something to do with mutations otherwise inducing mutations by exposing organisms with x-rays or gamma rays would not affect mutation rates.

Yes. For example, of course DNA replication involves extensive bond breaking and bond formation. When the two strands of DNA separate, that involves breaking of various types of bonds. Joining triphosphate nucleotides together, in an enzyme catalyzed reaction, to form the daughter strand involves formation of bonds. The amount of energy involved in the formation of these bonds is known to a high degree of accuracy. If the numbers aren’t in the article go to the citations. http://en.wikipedia.org/wiki/DNA_replication

But here’s where I think you’re misunderstanding…

1) As I previously pointed out, despite being diverse, mutations are also all kind of similar in terms of chemical energies involved. And the kinetics and thermodynamics of the reactions are not what makes them mutations. As John Harshman points out, an enzyme catalzying the simple addition of GTP where the template indicates that there “should” be an ATP might not have any energy implications to speak of (either event would have extremely similar kinetics and thermodynamics). Yet that mutation might have a major effect on phenotype. A duplication of a “parasitic” self-duplicating element many base pairs long would be a reaction that would consume more energy. Yet that could have no impact on phenotype. It’s where the mutation hits and what it does that matters most.

Neither the individual kinetics or thermodynamics of a mutation event, nor the probability of a given type of mutation occurring at a given site during a given replication, seems to have a strong relationship to effect on phenotype or implications for speciation. This is not a 100% dogmatic statement. It’s just what fits the data best right now.

I suspect that the truth may be slightly more complex, and that individual “big” mutations may, in the cases where they don’t result in death or infertility, contribute to genetic isolation, but the complex truth would still be very close to what the rest of us are saying, than to the idea that especially improbable single mutations drive speciation.

Part 2) later.

Let me try to divert this thread back onto the subject. (There will be nothing about chemical bonds in this comment).

I am impressed with the wonderful genes evo-devo people have found, and the comparisons of the functioning of those genes in different species. It is many remarkable stories, and has greatly improved our understanding of the evolution of development and of the resulting morphology.

But here’s what doesn’t impress me:

1. Statements by evo-devo people that evo-devo has made the Modern Evolutionary Synthesis obsolete. If you work in evolutionary biology, you are familiar with the annoying phenomenon of the self-promoting young person (let’s call him Sam Blotz) who discovers some nice stuff, then announces that this means that the Modern Synthesis is dead. The implication is that we have now entered the brave new world of its replacement, the Blotzian Synthesis. The problem with all this churning of paradigms is that the general public will draw the wrong conclusion from this – that all the stuff they have been told, that random mutation provides the raw material, and that the natural selection is why we see the choice of mutants that are adaptive, that all of that is now seen to be wrong. That we were ignoramuses and that we have to go back to Square One. Which is a high price to pay for stroking Blotz’s ego and promoting his career. Have evo-devo people succumbed to this temptation? En masse?

2. Leaving the impression that evolution “happens” because of mutations (and duplications and deletions) in these developmental genes but that natural selection is not involved.

3. Leaving the impression that these genes that have mutations of large effect are the whole story, that mutations of smaller effect, in those genes or elsewhere, play no role.

4, Leaving the impression that we didn’t understand evolution up till now, but now (thanks to the work of the marvellous Sam Blotz) we finally understand evolution.

5. Leaving the impression that evo-devo is the only really important phenomenon in evolution, which implies that organisms that aren’t multicellular don’t actually evolve (I do know that unicellular protists and prokaryotes do have processes that can be called developmental).

I am making a gross caricature of the statements of evo-devo people here. PZ’s talk, and his post, were brave attempts to balance the scales and to point out the the relevance of populational processes. I hope to be told that his attitude is typical, that the situation is not nearly as bad as I have implied, that no major evo-devo people are actually saying things like this. I’d be happy to be wrong.

The “Sam Blotz” phenomenon is hardly unique to evo devo, or even especially attached to evo devo. The death of the modern synthesis has been regularly announced since at least 1973, and I’ll bet long before then. Punctuated equilibria destroys it; so do symbiosis, group selection, neutral evolution, sexual selection…have I missed any? Come to think of it, didn’t mendelian genetics and mutation supposedly destroy Darwinism well before the modern synthesis? If I have a hammer, then it naturally follows that all problems are nails. Nothing new here.

harold said:

Part 2) later.

I appreciate the explanations, Harold.

I’ve just entered an extremely busy period for the coming months involving travel and a lot of projects that have to get done. So I am finding it a bit hard to concentrate on this.

I shouldn’t have brought up something that is off topic and for which I have so little time to focus on.

But thanks anyway.

Joe Felsenstein said:

Let me try to divert this thread back onto the subject. (There will be nothing about chemical bonds in this comment).

I am impressed with the wonderful genes evo-devo people have found, and the comparisons of the functioning of those genes in different species. It is many remarkable stories, and has greatly improved our understanding of the evolution of development and of the resulting morphology.

But here’s what doesn’t impress me:

1. Statements by evo-devo people that evo-devo has made the Modern Evolutionary Synthesis obsolete. If you work in evolutionary biology, you are familiar with the annoying phenomenon of the self-promoting young person (let’s call him Sam Blotz) who discovers some nice stuff, then announces that this means that the Modern Synthesis is dead. The implication is that we have now entered the brave new world of its replacement, the Blotzian Synthesis. The problem with all this churning of paradigms is that the general public will draw the wrong conclusion from this – that all the stuff they have been told, that random mutation provides the raw material, and that the natural selection is why we see the choice of mutants that are adaptive,that all of that is now seen to be wrong. That we were ignoramuses and that we have to go back to Square One. Which is a high price to pay for stroking Blotz’s ego and promoting his career. Have evo-devo people succumbed to this temptation? En masse?

2. Leaving the impression that evolution “happens” because of mutations (and duplications and deletions) in these developmental genes but that natural selection is not involved.

3. Leaving the impression that these genes that have mutations of large effect are the whole story, that mutations of smaller effect, in those genes or elsewhere, play no role.

4, Leaving the impression that we didn’t understand evolution up till now, but now (thanks to the work of the marvellous Sam Blotz) we finally understand evolution.

5. Leaving the impression that evo-devo is the only really important phenomenon in evolution, which implies that organisms that aren’t multicellular don’t actually evolve (I do know that unicellular protists and prokaryotes do have processes that can be called developmental).

I am making a gross caricature of the statements of evo-devo people here. PZ’s talk, and his post, were brave attempts to balance the scales and to point out the the relevance of populational processes. I hope to be told that his attitude is typical, that the situation is not nearly as bad as I have implied, that no major evo-devo people are actually saying things like this. I’d be happy to be wrong.

Joe,

I absolutely agree with this, as long as you also take into account that there are also those who are attempting to integrate the fields of evo-devo with the fields of population genetics and ecology. These efforts are primarily aimed at extending the evolutionary synthesis rather than replacing it. Just as modern genetics extended our understanding of basic evolutionary processes, the new synthesis also has the potential to revolutionize our understanding. Of course, it doesn’t mean that evolution was wrong any more than the first synthesis did, did it just means that we are learning more every day. Here are a couple of references for anyone who is interested (others should feel free to add to the list):

Evo-devo: Extending the Evolutionary Synthesis. Nature Review Genetics 8:943-949 (2007)

The Locus of Evolution: Evo Devo and the Genetics of Adaptation. Evolution 61(5):995-1016 (2007)

Mike Elzinga said:

harold said:

Part 2) later.

I appreciate the explanations, Harold.

I’ve just entered an extremely busy period for the coming months involving travel and a lot of projects that have to get done. So I am finding it a bit hard to concentrate on this.

I shouldn’t have brought up something that is off topic and for which I have so little time to focus on.

But thanks anyway.

Anyway, Mike, here is “part 2” of my comment, and it also has nothing (directly) to do with chemical bonds.

The other thing you may have been getting a little hung up on is the level of reduction.

As an anaology, when I was working as a pathologist, I used light microscope level techniques constantly. I essentially never used electron microscopy.

Do I deny the existence of electron microscopy? No. Do I dislike electron microscopy? No, quite the contrary. Is electron microscopy useless for the clinical practice of pathology? No, on the contrary, it’s valuable for some problems in pathology, just not the ones I was working with. It was tested and found not to be very contributory in the past. Later, new techniques that were helpful came along.

I did, however, make use of data from PCR based molecular diagnostic techniques, quite frequently, even though that is a level of greater reduction that electron microscopy.

No-one denies the importance of atoms and chemical bonds, it’s just that, when we talk at the level of molecules and phenotypes, we don’t need to dwell on what is already known about the biochemical kinetic and thermodynamic level.

Your extremely valuable efforts against creationist distortions of physics (and basic logic) are greatly appreciated.

These efforts are primarily aimed at extending the evolutionary synthesis rather than replacing it. Just as modern genetics extended our understanding of basic evolutionary processes, the new synthesis also has the potential to revolutionize our understanding. Of course, it doesn’t mean that evolution was wrong any more than the first synthesis did, did it just means that we are learning more every day

Exactly. There is always a tendency for people to insist that extending and clarifying something is the same as “replacing” it.

Most of the time it’s a semantic issue.

However, in the case of scientific facts that are dishonestly disputed by people with ulterior motives, it can be very distracting. To use an example not directly related to evolution, if an allele that made some people even more susceptible to some health consequence of cigarettes, than the general population is, was discovered, cigarette company shills might make the irrational claim that exceptionally well-established and conclusive research on cigarettes and health had been “overturned”, and that health problems highly associated with cigarettes were “entirely genetic”, or some such thing.

A similar situation exists in fields directly related to evolutionary biology, as whenever an important discovery strengthens, expands, and clarifies our understanding, ID/creationists will inevitably argue “something new, therefore everything that is already known must be false”.

This comment has been moved to The Bathroom Wall.

Thanks PZ for this thoughtful article.

Paul Burnett, if you haven’t given up on the whole thing, first, speciation does not generally happen due to one big mutation, nor are species generally separated from one another by a single large mutation. I think you misunderstood something back in high school. Don’t worry, you wouldn’t be the first. Speciation, especially in animals, is likely to be gradual, but this does not mean that it must take a long long time. Small mammals like tree rats or perhaps even small primates in tropical forests may be speciating as we speak.

Hybridization may sometimes lead to a new species. Environmental opportunities such as insects and plants finding each other (that hadn’t before) can lead to new species. Genome duplication may result in new species. etc etc.

Here is one instance of rapid speciation in salt marsh cord grass: http://ecobio.univ-rennes1.fr/Fiche[…]Ainouche.pdf Genetic and epigenetic consequences of recent hybridization and polyploidy in Spartina (Poaceae)

Mike Elzinga said:

The actual complete speciation would have to occur at a level that is chemically more tightly bound than the levels of actual development where the binding energies are much smaller (0.01 eV as compared to 1 eV).

This is true of all complex systems that are comprised of increasingly complex and increasingly more loosely bound systems built on top of a more robust “core” that provides an underlying template.

So it should not be surprising that changes in the frequencies of alleles affecting development would gradually isolate populations until “the big but rare event” that affected the “core” made interbreeding impossible.

This alone should highlight a problem with Darwinian chance. The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

petedunkpi said: Paul Burnett, if you haven’t given up on the whole thing, first, speciation does not generally happen due to one big mutation, nor are species generally separated from one another by a single large mutation.

Thanks for your patience. That’s not what I said (“big”) - I was cleaning up Mayr’s accusation that Goldschmidt believed that “new species…arise by a single fortuitous macromutation in a single individual…” by crossing out “macro.” I understand that most mutations are damaging, neutral or slightly beneficial - only a few are “fortuitous” and it takes several fortuitous mutations in a population to ratchet into a different species. The point I was attempting to make is that only an individual can “get” a mutation - a population doesn’t “get” a mutation in a single generation. Right?

Ian Brandon Andersen said: The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

Please provide us with a few examples of this happening in a genomic sequence. Or even one example.

I have to say that I was one of the initial naysayers of Harshman when he mentioned bond energies in the context of mutation rates. I’ve learned a tremendous amount of biology in the meantime, in very large part to many of the comments posted here. So:

John Harshman: I apologize for my initial outburst, and I appreciate your patience (and that of the other PTers) in explaining the situation as currently understood in the laboratory.

Paul Burnett said:

Ian Brandon Andersen said: The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

Please provide us with a few examples of this happening in a genomic sequence. Or even one example.

Isn’t it obvious? The higher the bonding energies, the greater amount of energy it takes to them. Since the energy to break said bonds must directed at them, this lowers the probability this could occur by random chnce.

Ian Brandon Andersen said:

Paul Burnett said:

Ian Brandon Andersen said: The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

Please provide us with a few examples of this happening in a genomic sequence. Or even one example.

Isn’t it obvious? The higher the bonding energies, the greater amount of energy it takes to them. Since the energy to break said bonds must directed at them, this lowers the probability this could occur by random chnce.

Yes, it certainly does and good thing for you. If the mutation rate were any higher, you would be subjected to even more problems. But of course, no intelligence is needed to direct mutations and none has been detected, just as none is detected in your comment.

Ian Brandon Andersen said: Isn’t it obvious? The higher the bonding energies, the greater amount of energy it takes to them. Since the energy to break said bonds must directed at them, this lowers the probability this could occur by random chnce.

Provide an example.

Ian Brandon Andersen said:

This alone should highlight a problem with Darwinian chance. The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

You appear to be arguing that cosmic rays are a product of intelligent design.…

Kevin B said:

Ian Brandon Andersen said:

This alone should highlight a problem with Darwinian chance. The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

You appear to be arguing that cosmic rays are a product of intelligent design.…

And UV radiation. Interesting. That would make the sun an “Intelligent Designer”.

harold said:

Kevin B said:

Ian Brandon Andersen said:

This alone should highlight a problem with Darwinian chance. The higher the binding energies, the less likely they will randomly break, for higher levels of energy need to be directed by intelligent design.

You appear to be arguing that cosmic rays are a product of intelligent design.…

And UV radiation. Interesting. That would make the sun an “Intelligent Designer”.

Well you know the photons are bend by the magnetic field of the earth, creating an a magic invisible hologram that directs development of every organism. So yea, I guess the sun must be the intelligent designer. Funny, those pagans had it right so many thousands of years ago.

I get the impression that this discussion is assuming that “random chance” means that all possibilities have an equal probability of happening. As far as I understand the mathematics of probability (and I am not a mathematician), this is not the case. Am I wrong, or am I misunderstanding the discussion?

TomS said:

I get the impression that this discussion is assuming that “random chance” means that all possibilities have an equal probability of happening. As far as I understand the mathematics of probability (and I am not a mathematician), this is not the case. Am I wrong, or am I misunderstanding the discussion?

Ian Brandon Andersen is a somewhat amusing parody troll who is either the same person as, or highly similar in style to, Higaboo Andersen and Toidel Mahoney.

However, let’s talk about what “random” means.

In math and science, it does not usually mean “anything can happen with equal probability”. It is usually used to describe situations which are quite different from this.

A random variable exists when you can select something from a distribution, but you can’t predict exactly what you will select, even if you can fully characterize the distribution.

A random variable has a probability or frequency associated with it.

An example of a random variable is the sum you get when you throw two dice. It can only be an integer between two and twelve. It is much more likely top be some numbers than others. For example it is more likely to seven than to be twelve (six times more likely). This is an example of a completely understood, discrete, bounded distribution. Nevertheless, you cannot predict which number you will get next*. And not all numbers are equally probable. *There is a school of thought, which I personally scornfully reject, which claims that rolling dice in a certain way can influence the outcome. However, even if this were true, they would not claim to be able to perfectly predict the next number, so the example stands and we can ignore this issue.

Genetic mutations are very much random, in the sense that they are extremely well modeled as random variables. Some are more common than others, and we have a good idea what the frequency of many of them is, in terms of generations or time. However, when DNA replicates, we can’t perfectly predict which mutations will occur.

As for this -

Isn’t it obvious? The higher the bonding energies, the greater amount of energy it takes to them. Since the energy to break said bonds must directed at them, this lowers the probability this could occur by random chnce.

In isolation, this statement borders on being correct, but is too oversimplified to be fully evaluated. For example, some highly spontaneous reactions may have an associated “energy of activation”; is some cases, for example, you could mix ingredients that would be inert at room temperature, but end up with a smoking crater where the lab used to be if you were foolish enough to heat the mixture up beyond a certain critical temperature, without taking proper precautions. Simply because a reaction will result in a net local increase in heat does not mean that it is probable that it will occur. More to the point, biochemical reactions are typically catalyzed by enzymes. http://en.wikipedia.org/wiki/Catalyst

Furthermore, even if it were true that all chemical reactions always had a probability of occurrence directly related to the energy needed to initiate or maintain the reaction, this would not imply magic.

Indeed, anyone who uses the term “improbable” to mean “impossible” or “requiring magic” is either a parody troll indulging in the lottery fallacy, as “improbable” by definition implies “could happen”.

As I pointed out earlier, 1) the kinetics and thermodynamics of the chemical reactions that represent mutations occur within a narrow range, and are not much different, in some cases probably not different at all, from the kinetics and thermodynamics of replicating a segment of DNA without a mutation and 2) although the “size” of a mutation is probably mildly associated with effect on phenotype (remembering that “failure of an unviable zygote to develop beyond early embryo stage” is still technically a phenotype), a point mutation can have a huge impact on phenotype, and a large insertion or deletion can have no impact whatsoever.

Joe Felsenstein said: I am making a gross caricature of the statements of evo-devo people here. PZ’s talk, and his post, were brave attempts to balance the scales and to point out the the relevance of populational processes. I hope to be told that his attitude is typical, that the situation is not nearly as bad as I have implied, that no major evo-devo people are actually saying things like this. I’d be happy to be wrong.

PZ Myers should be ridiculed at every opportunity.

Atheistoclast said:

PZ Myers should be ridiculed at every opportunity.

And you, I’m sure, know just what that feels like.

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This page contains a single entry by PZ Myers published on February 22, 2012 2:29 PM.

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