Stephen Jay Gould died ten years ago on May 20, 2002. Last month there was a conference in Venice, Italy, that celebrated his legacy [Stephen J. Gould's Legacy: Nature, History, Society]. I wish I could have attended because all the main characters were there (Richard Lewontin, Niles Eldredge, Elisabeth Lloyd, and many more). Ryan Gregory gave a talk on A Gouldian view of the genome and he has posted the video of his presentation (see below). I urge you to watch the whole thing but, if you only have a few minutes, then watch the beginning where Ryan describes the important lessons that Gould taught us.
- Narrative: The details of "pure history" are important.
- Origins: The reasons a trait first evolved and why it still exists may be different.
- Exaptation: Features can become co-opted to serve new functions.
- Development: The connections between genotype and phenotype are important
- Pluralism: Small genetic changes accumulating slowly over time due to natural selection is not all there is.
- Contingency: Unique events can have a large influence in the long run, even if they seem minor initially.
- Hierarchy: Evolutionary processes can occur at multiple levels.
- Scholarship: Know the history of one's field.
I'm sure Gould would have enjoyed learning more about genomes. Here's what he wrote in The Structure of Evolutionary Theory (p. 22). You'd be hard pressed to find any other prominent evolutionary biologist who writes so frankly about his strengths and limitations.
But I recognize that every strength comes paired with weaknesses. In my case, a paleontological focus leads me into relative ignorance for an equally important locus of reform in the structure of Darwinism—increasing knowledge of the nature of genomes and the mechanics of development. (I try to cover the outlines of important theoretical critiques from the "opposite" realm of the smallest, but the relative weightings in my text reflect my own varying competencies far more than the merts of the case. For example, although I do discuss, and perhaps even adequately outline, the importance of Kimura and King's neutralist theory in questioning previous assumptions of adaptationist hegemony, I surely do not give an appropriate volume of attention to this enormously important subject.)
24 comments :
All of the talks will be online soon. Note that Lewontin provided his via pre-recording, but the others were all there in the flesh. :-)
Evolution is such a huge and complex topic that it's probably not humanly possible for any one person to understand even the little we'll ever know about it. No one will ever have more than a partial view of it, no matter how much of contemporary knowledge they've mastered.
You've got to wonder what it means to understand a subject like that, if any person can meaningfully be held to be "literate" in it.
Gould was a nice guy. I met him a few times. Lewontin, too.
Intersting --- what happened to the "third musketeer" Elisabeth Vrba??
She's here.
"Stephen Jay Gould died ten years ago on May 20, 2012."
Ummm. May I suggest you to rephrase it?!
... and by the same token, to correct the title...
As an example I just happened upon, there's the recent online skirmish between Jerry Coyne and James Shapiro, which I can sort of, kind of, get when it touches on the several things I've read up on before but, when you look at comment threads in the dueling blog posts, it's clear exists for most people as more of a sports competition with opposing champions instead of matters of science. I suspect that the blocks the two sides construct their arguments out of are so complex that even the two informed parties in the argument are finding it hard to manage them. For almost all of the rest of us, it's impossible to have a legitimate view of it. Though I'll say from what I can understand I'd bet on the post-neo-Darwinians as being pointed in the direction of the future.
Coyne's lack of discipline and clear appeal to prejudice, in holding up his side, might appeal to blog fans, it's something I associate with not having a valid argument.
Lewontin has pointed out that even some of his colleagues at Harvard, in his own department, would have trouble understanding general points relevant to his work. I seem to recall he said they'd be about as prepared to discuss that as the general readership of the New York Review. But when you're talking about evolution as a general phenomenon in nature, things you aren't going to understand but that can be understood by other specialists, are inevitably relevant to the topic. I'd bet that becomes more true as more is learned instead of less and that a lasting synthesis will be increasingly unlikely.
Just call me skeptical.
I was concerned at first, but by the end of the video Ryan Gregory shows himself to be a good adaptationist. There Gregory’s diagram shows, correctly, ecology and natural selection at the top of the causal hierarchy. At 31:40 Gregory cites Gould (1995) as interpreting evolutionary stability (e.g., C-values) as a balance or tradeoff of opposing hierarchical selection pressures. However, this is the exact opposite view that Gould and Lewontin took in their 1979 spandrels paper, which captured the everlasting esteem of New Age lab scientists. Here G&L caricature the Adaptationist Programme – a realm of mere field biology – as the product of “faith in the power of natural selection as an optimizing agent.” “It proceeds,” they affirm, “by breaking an organism into unitary 'traits' and proposing an adaptive story for each considered separately. Trade-offs among competing selective demands exert the only brake upon perfection; non-optimality is thereby rendered as a result of adaptation as well. We criticize this approach . . . ” Thank you Ryan Gregory for the (unintentional)irony!
The correspondence between Gregory’s slide at 13:30 in the video, describing the extremely small C-values of hummingbirds (a most perceptive hypothesis pulled from quintessential adaptationism) as possibly due to “jettisoned . . . genomic baggage” is uncannily similar to a somewhat earlier statement by Ernst Haeckel in reference to selection for the adaptive loss of junk anatomy: “It is easier to fight [compete],” says Haeckel, “when useless baggage is thrown aside.” (Haeckel, 1876, The History of Creation, 4th edition, vol. 1, p. 286 – German edition 1873). Are there writings earlier than 1873 proposing that natural selection eliminates junk traits? Poor Gould: wrong, self-contradictory, and 100 years late.
Less Polite, More Bite.
I enjoyed Ryan’s talk, and looking forward to listen to the other tributes to Gould’s work. Gould’s lessons as presented by Ryan are highly relevant; however, it would be great to have an outline or a list of his major original scientific contributions, if possible in order of their significance.
However, this is the exact opposite view that Gould and Lewontin took in their 1979 spandrels paper, which captured the everlasting esteem of New Age lab scientists.
Actually, at the time the New Agers were all verklempt over sociobiology, which morphed into evolutionary psychology. The idea of selfish genes and a simple evolutionary explanation of altruism have much more New Age flavor than complex ideas like pluralism, punctuated equilibria, Neutral Theory, and random genetic drift.
New Agers like explanations to be as simple as possible. That way they don't risk hurting their brains.
Poor Gould: wrong, self-contradictory, and 100 years late.
What was he wrong about? Do you have an adaptationist explanation for the presence of massive amounts of junk DNA in our genome? If so, I'd love to hear it.
I wondered about that. I'd don't think Lewontin likes to travel.
How was Venice?
... I'd bet on the post-neo-Darwinians as being pointed in the direction of the future.
I agree with you and, therefore, I disagree somewhat with Jerry Coyne. However, there are many flavors of "post-neo-Darwinism" and I'll bet on the Gould viewpoint.
Shapiro has no idea of the recent history of evolutionary theory—there's no mention of Gould in his book—and his view of evolution is certainly wrong. Don't bet on finding the name of James Shapiro in future textbooks.
The idea of selfish genes and a simple evolutionary explanation of altruism have much more New Age flavor than complex ideas like pluralism, punctuated equilibria, Neutral Theory, and random genetic drift.
Yes. Yes it does. I've never seen an idiotic, foolish, incoherent citation of spandrels, pluralism.... on blog comment threads. That can be contrasted to the ubiquitious Dawkinsian buzzwords and drivel that does so much to substitute for thinking and dangerously infects political discourse and reporting.
The reason is that Dawkinsism is based in simple narrative, Gould and Lewontin are based in things that require more knowledge beforehand. Genetic Drift might, eventually, turn out to be a far more powerful explanatory idea than Dawkins' vulgarization of Darwinism but it will never be compellingly represented in a popular TV show.
Which is why science should dump the condescending attempts to explain evolutionary science with costume dramas and ethological folk lore which do at least as much to distort as they do to convince.
Larry Moran: Do you have an adaptationist explanation for the presence of massive amounts of junk DNA in our genome? If so, I'd love to hear it.
Two decades ago I published a paper entitled “A protective function for noncoding, or secondary DNA” (Med Hypotheses, 31:33-4, 1990). The paper is very short and it is behind a pay-wall, so I’ll post it below (the references are not included, but for those interested, I can provide a PDF copy; send me an e-mail at: cbandea(at)cdc.gov).
Introduction
A high percentage of eukaryotic DNA, more than 99% in some species, makes no apparent phenotypic contributions. The following mechanisms have been proposed for the origin of this noncoding, or secondary DNA: (i) the ‘accidental’ duplication of some genomic sequences during DNA replication and recombination, (ii) the spread of some genomic sequences through retro-transposition, and (iii) the spread of proviruses and transposons.
It is not known if secondary DNA has accumulated simply because its rate of deletion has been lower than that of origin, or because individuals possessing secondary DNA have a selective advantage.
A protective role for secondary DNA
I propose that secondary DNA functions as a sink for the integration of proviruses, transposons and other inserting elements, thereby protecting coding sequences from insertional inactivation or alteration of their expression. Assuming a random site for integration, a genome containing a high percentage of secondary DNA is less prone to insertional damage. This protective mechanism would be more efficient if inserting elements were targeted to secondary DNA. A putative targeting mechanism is homologous recombination. As mentioned, secondary DNA contains sequences that originated from inserting elements. Perhaps, these sequences can direct recombination with homologous sequences from actively transposing parental and related elements.
In addition to its hypothetical protective function, secondary DNA has probably influenced the evolution of cells and their genome, For instance, to accommodate secondary DNA, cells have changed their metabolism (e.g. nucleotides metabolisms) and structure (e.g. nuclear volume). Secondary DNA may have also influenced the rate of evolution by increasing genome fluidity.
The protective function of secondary DNA would make evolutionary sense only if insertions occur at a relatively high frequency. The presence of numerous inserted elements in eukaryotic genomes is evidence that insertions in the germ line are common. Insertions at the somatic level, however, probably occur at much higher frequency in a multicellular organism. In the absence of a protective mechanism, these insertions could lead to high incidents of neoplasmic transformation by altering the expression of some cellular genes. Secondary DNA may also prevent viruses from becoming oncogenic by reducing the probability that host genes having oncogenic potential are incorporated into viral genome.
The advantage in having a protective mechanism against insertions is perhaps best illustrated by organisms that do not have much secondary DNA. Some bacteria and their prophages have coevolved specific sequences where integration occurs, thereby protecting genic sequences.
Conclusion
This paper proposes that secondary DNA was selected as a protective mechanism against insertional damage and suggests that experimental genomic integration of sequences homologous to those of actively inserting elements would enhance the protective function of secondary DNA.
"at the time the New Agers were all verklempt over sociobiology, which morphed into evolutionary psychology."
Excuse me, Professor Moran, but at the time, the loudest squawking about sociobiology, at least freom inside biology, was actually coming from none other than Lewontin and Gould.
I don't think you could accuse Gould of being a New Ager, he was publicly opposed to a lot of that. Nor Lewontin, who they were always accusing of being unreliable on the basis of his being a commie. Against Sociobiology was hardly a new ager tract. I wouldn't have put that the way LM did but the substance of his statement is as I recalled it and as it still is.
Chas Peterson said,
... at the time, the loudest squawking about sociobiology, at least freom inside biology, was actually coming from none other than Lewontin and Gould.
That's correct. They opposed the New Age adaptationist view of sociobiology.
Organisms with small compact genomes have very few transposons. New transposons will likely inactivate a gene and the individual will die. This will be a very rare event.
You are proposing that individuals with such genomes will gain a selective advantage by increasing the size of their genome. The "advantage" is a future advantage that will only affect a tiny percentage of its offspring several generations later.
How would that work?
Also, please explain how your explanation passes The Onion Test.
Claudiu Bandea Assuming a random site for integration, a genome containing a high percentage of secondary DNA is less prone to insertional damage.
But since much of the secondary DNA is buried in heterochromatin, it is less accessible than the actively transcribed fraction - it creates all this sacrificial DNA and then sticks it where the insertional elements can't get at it?
Larry Moran: Organisms with small compact genomes have very few transposons. New transposons will likely inactivate a gene and the individual will die. This will be a very rare event.
Organisms with small compact genomes have relatively few transposons for a good reason: a very strong selection against extra-DNA in their genome. However, the evolution of protective mechanisms in these organisms in form of specific integration sites for transposons and phages is testament for the strong selective pressure against insertion mutagenesis.
Larry Moran: The "advantage" is a future advantage that will only affect a tiny percentage of its offspring several generations later. How would that work?
The following excerpt from a more recent paper (http://precedings.nature.com/documents/3888/version/1)might partially address your question:
“Early on, during the evolution of this protective mechanism, when there was little ncDNA, there were probably enhancing mechanisms such as recombination (79), which could have targeted the integration of the viral genomes in host genomic regions containing homologous viral ncDNA sequences. It is highly probable, therefore, that some of the recombination machineries evolved at least partially to facilitate the insertion of invading viral genomes within the host chromosomal regions containing ncDNA, which enhanced the protective role of ncDNA.”
Larry Moran: Also, please explain how your explanation passes The Onion Test
The Onion Test seems to be a formidable and high inconvenient query. No wonder why it has yet to make it into the peer reviewed scientific papers and textbooks! Obviously, I ‘ll need to address it in context of my hypothesis, and I hope to do that soon.
Allan Miller: But since much of the secondary DNA is buried in heterochromatin, it is less accessible than the actively transcribed fraction - it creates all this sacrificial DNA and then sticks it where the insertional elements can't get at it?
Good point! However, there is plenty of ncDNA in actively transcribed regions, including the introns. Also, it is very likely that some of the ncDNA acquired additional new functions, such as those associated with heterochromatin.
I can't see the video, it's labeled as private. Is there any place I can watch it?
Claudia Bandeau, before I respond to your idea I want to repeat it in my own words to find out whether I understand it.
First, the problem: lots of DNA is noncoding, and the question is whether this is there because it accidentally gets created more than it gets deleted and there is no particular selection involved, or whether it in some way provides a selective advantage.
You briefly mention ways that noncoding DNA might be selective, for example "increasing genome fluidity", and settle on a primary role of protection against various things that damage DNA. The idea is simple: If something can damage a limited amount of DNA, then the more dummy DNA you provide for it to damage, the less the important DNA will get damaged. Kind of like dummy nuclear warheads for ICBMs.
You specifically talk about inserting elements, but the same reasoning works for free radicals or other mutagens. Anything that damages DNA at a single site, will do only 1% the damage if you provide it with 99 dummy sites for every important site.
Well, but why not instead have more good copies? If you have 2 copies of your genome, and if you can tell which one is damaged and splice a copy of the good version onto the bad version, then you do better than with just one good copy and one dummy. The more good copies you have, the better in general that you remove errors. If you want to save information on your hard disk, aren't you better off with 50 good copies than with one good copy and 49 times as much gibberish?
Well, maybe. If sometimes instead the bad copy spreads uncontrollably, it can kill you. You mentioned cancer in multicellular organisms. Similarly if a unicellular organism gets a mutation that doesn't merely destroy a gene's function but perhaps eliminates its control and produces its product without limit? That can be deadly too. Noncoding DNA that just sits there might be better.
So I think your idea could be true. I imagine that better ways to achieve the same function would have evolved, but I can't really predict evolution all that well.
Claudia Bandeau, could noncoding DNA arise from some other selection?
Could insertions have a selective advantage? Maybe not proviruses, which can spread faster than they kill off their hosts. But insertion sequences that rarely travel? If they do damage, they are selected to do something valuable to compensate, because they survive with their hosts. If they are valuable it does not pay to get rid of them, leading to selection to palliate their bad effects.
Could insertion sequences aid selection? Sure, in theory. Eucaryotes rarely develop entirely new capabilities, they adapt by doing the same things in different amounts and different circumstances. We usually use existing capabilities in new ways to better fit our ecological niches. Rarely we use existing capabilities to fit new niches. Extremely rarely we develop brand new abilities that fit new niches. If insertions can change the pattern of regulation, they can improve it. To do that they must insert somewhere that matters, probably somewhere noncoding. Or at least not protein coding. Easier to change a protein’s regulation than to join pieces of two protein domains and get a functional domain.
Insertions could become adapted to improve adaptation. For a trivial example, if some insertions could create a generic method to make nearby genes dominant or recessive. (RA Fisher proposed this many years ago assuming dominance modifiers that changed as slow as the genes they modified. That’s oo slow.)
If much of adaptation is regulatory change, and regulatory changes can happen at specific sites mediated by insertions, which mutations tend to be selected? Mutations at the same sites as previously-selected mutations, or random mutations? When a previously successful insertion is deleted, why not leave a landing strip behind for future insertions?
If this works, we are all descended from the individuals that got jackpot events where it worked great. Our ancestors were not the individuals that were killed by the process. It doesn't have to work very often to be selected, unless the failures drive down the population size. But if insertions at sites of previous successes are more likely to be successful, it would be bad to have lots of random useless insertion sites. Hide them away with heterochromatin etc, if you can guess which ones to hide.
If the process is selected but many insertions have little effect, how important is it to delete them? How do you tell the good ones from the neutral ones? I've been fantasizing extremely sophisticated functions for insertions that would require hypothetical advanced molecular mechanisms, but that one is too far even for me. If there's selection to make them and little selection to delete them, then there we are. As a first approximation a cell with 1000 times the volume might support 1000 times as much DNA.
I could propose a method that insertions might use to estimate their frequency in the population. Populations evolve faster when they have more variation in fitness. When they have little variation they will probably not have much variation in fitness. Genes that could estimate variation at their loci could then do insertions when variation is low. With such a mechanism, larger populations could maintain genetic diversity even after selection events, and could reliably evolve faster. In the process they might accumulate insertions faster.
It's easy to imagine selection for these elements, if you assume molecular mechanisms which have not been observed but which are not implausible either. If evolution selects mechanisms that speed adaptation, then plausibly such molecular mechanisms might evolve. In each case the mechanism might fit a series of other adaptations before it achieves the capabilities needed for a specific approach to faster adaptation of other genes.
Post a Comment