Reuters is reporting that a senior politician in Ireland suggests that they make the switch from driving on the left side of the road to right-side driving, in light of the dumb tourists from North America and continental Europe who cause accidents.
I don’t know what the Irish think about this, but I recommend phasing it in gradually like they did in Newfoundland in 1947, starting with just the large trucks.
Anyone who reads this blog but not Sandwalk (if any) should go right now and see Larry’s posts on junk DNA. Although I do not care so much for the term “junk DNA” because often it is employed ambiguously, Larry is careful to define it explicitly as sequences for which the evidence indicates nonfunction. The posts on the distinct components of the genome that are considered junk under this definition are:
Junk in your genome: pseudogenes
Junk in your genome: protein-encoding genes
A collection of related posts is compiled under Theme: genomes and junk DNA.
Enjoy!
So I am reading Neil Shubin’s Your Inner Fish, which as noted I was eagerly anticipating. My immediate reaction is that it will be a good little book for non-experts, but the very basic overview of topics and stilted writing style (think of the exact opposite of Stephen Jay Gould’s long, comma-filled, complex sentence constructions) will be less engaging to biologist readers. I suspect that I do not reflect the target audience, though, so no major complaint here.
The title of the book refers to species such as Tiktaalik roseae (which Dr. Shubin and his colleagues discovered, to much deserved acclaim), an extinct species that, in retrospect, held characteristics that we may consider transitional between fishes and terrestrial tetrapods. Whereas Tiktaalik itself is probably not a direct ancestor of ours, I don’t have much of a problem with the “inner fish” idea on the basis of this comparison. After all, we’re talking about extinct ancestors (or things similar to ancestors) that were fishes and from whom we have inherited some persistent characteristics despite the many changes that have occurred in our lineage.
But then on p. 59, in a discussion of developmental regulatory genes which are similar in sequence and effect in different model organisms, we find:
An “inner fly” helped find an “inner chicken”, which ultimately helped Randy [Dahn, one of Shubin’s students] find an “inner skate”. The connections among living creatures run deep.
Here is a phylogeny of the organisms being discussed, all of them modern species:
At no time was there a fly in vertebrate ancestry. There was no skate in the ancestry of terrestrial vertebrates. The ancestral amniote was not a chicken. (And, while we’re on the subject, the ancestor of humans was not a chimp). There is a common ancestor shared by all of these contemporary animals, but it was not a fly any more than it was a human. Humans do not have inner flies — and equally, flies do not have inner humans. If anything, both have an “inner-common-ancestor-of-metazoans”, but admittedly that is more accurate than it is memorable.
Dr. Janet Stemwedel is a philosopher at San Jose State who also happens to have earned her PhD in physical chemistry, which means she has some significant street cred when discussing science. Her blog is known as Adventures in Ethics and Science, and recently she began a series on being a grown up scientist. Part 1 identifies some of the many things that professional scientists must do that graduate students are not taught, or may not even be aware of, while they are in training.
Of course, what I discovered is that there is a great deal more one needs to learn than just how to be creative, have good insights, design reasonable experiments, present reasonable data, and write clear scientific papers. (Even this much is quite a lot to learn, and some of it — like scientific creativity — is pretty hard to teach.)
Grown-up chemists also seemed to know how to write effective grant proposals, how to manage (and even mentor) graduate students, postdocs, and technicians, how to nurture productive and mutually beneficial relationships with other chemists in their sub-specialty, how to stay on top of the literature and discern which newly described results or techniques were most important (at least with respect to their own research area), how to be fair and constructive peer reviewers and how to respond effectively to referee reports on their own manuscripts, how to work within departmental politics and the politics of their discipline.
They knew how to tell when an experiment was done, when the data was good, when there was a finding that merited a paper to announce it. They knew how to work out authorship on the papers. They knew who, in their field of research, would be the hardest to convince of the new result. They knew which journal would be the best place to submit a particular manuscript and which meeting would be the best venue to present pre-publication results. And, they could conceive of three distinct follow-up projects to build on the new results.
Plus, they (at least, the grown-up chemists I was looking to as role models) seemed to know which chemists in the community were good people to talk to, collaborate with, or argue with (in the best sense of argument, where each side makes its best case and then presents its best criticisms of the other side). And they seemed to have identified the chemists around whom you’d want to watch your back.
Grown-up chemists had a huge body of unwritten knowledge to draw upon, it seemed. But hardly any of it seemed to be the focus of our graduate training — at least, not explicitly.
I must say I agree totally — there is a tremendous difference between being a grad student and being a professional academic scientist, but it’s probably the case that most of us do not realize that until we are faculty. I certainly had a profound new respect (in addition to an already considerable amount) for my former advisors when I became a professor myself.
Part 2 of Janet’s series will ask “Why don’t most advisors talk about the things grad students most want to learn from them?”. I am looking forward to the rest of her posts, and I recommend them to both students and advisors as the basis for discussion and thought.
Some readers might recall my comments from September 2007 regarding the “Bloggers for Peer-Reviewed Research Reporting (BPR3)”, in which I noted that I was not going to participate, at least for the moment. The reason was that I thought the name and icon that had been selected gave the misleading sense that the blog post itself had undergone review, not that it was simply about peer-reviewed research. As a scientist, I take the peer review system very seriously (its several problems notwithstanding) and I do not wish to see blogs perceived as even an approximation of that system. That said, blogs are a useful way to discuss research, and I am happy to see this new development in science communication.
The folks at BPR3 accepted my criticism, and I am pleased to note that the icon was quickly fixed. I also think the idea of an aggregator (ResearchBlogging.org) for posts on research articles is useful, so in principle I can see the utility of the idea.
The questions I had initially were: 1) will the icon give a false impression that the blog is reviewed? and 2) does such an icon really add anything, and can’t readers tell if a post is about a paper? I did not anticipate the third question that has now come up: 3) what will be done if the icon is used inappropriately by anti-evolutionists?
You can read about the situation that is happening right now with the icon and its misuse by a proponent of intelligent design here, here, here…
My response is simply to echo what some others have already said and to recommend that the following items be made prerequisites for gaining permission to use the BPR3 icon and aggregation service:
If anti-evolutionists or anyone else is willing to live by these rules in addition to those that already have been determined, then let them use the icon. Forcing them to open their comments and provide trackbacks will be a major improvement over the current situation. If BPR3 makes these further changes, I will probably start participating (I doubt they will do anything just on my behalf, but on the other hand they could probably use more professional researchers on their side, and I do not imagine that my view is unique among us).
And folks, let’s remember one other thing: it’s just an icon and an aggregator service and nothing more — it is not the arbitrator of what is good or official among scientific blogs.
Note – this post has been updated since originally posted.
In the recent exchange regarding my post about genome size and code bloat, one of the authors of the study in question made the following claim:
In its conclusion prof. Gregory suggests that we claim that “Non-coding DNA does
accumulate “so that” it will result in longer-term evolutionary advantage”.
We ABSOLUTELY NEVER stated such a non-sense. It is curious that the same accuse was moved by prof. Gregory in its article “Coincidence, coevolution, or causation? DNA content, cell size, and the C-value enigma”, that we cite in our paper, to an article by Jain that we also cite in our paper. So, either prof. Gregory has a very poor opinion of our intelligence, or he thinks that we do not read the articles that we cite. Let us state, unambiguously, what we and Jain really say: “IF does exist a mechanism for genome size increase, THEN maybe the resulting long-term advantage can overcome the short-term disadvantage” (Jain was referring to the selfish dna as the genome increasing mechanism while we do not give any preference). Prof. Gregory reverts the implication: “IF there is a long-term advantage THEN the mechanism of genome increase is the product of selection”, and then explains us that it can’t be true. Incidentally, in the case of Jain, I think that what he was really intending can be clearly understood just by the title: “Incidental DNA”.
When someone suggests that one has misinterpreted the claims of an author, the appropriate thing to do is to consult the original article to be sure. So, I looked up the Jain (1980) letter, some quotes from which are given here (with emphasis):
Natural selection is concerned not only with the existing variability but even more so with mechanisms which ensure its continued availability. If there is intragenomic selection leading to rapid build-up of some of the DNA sequences (the selfish DNA of Doolittle and Sapienza and Orgel and Crick) we must treat this part of DNA as incidental to the fundamental process of mutability so vital for ensuring continued supply of raw material for the production of new genes. It does not follow that all of the DNA produced in this manner will, in fact, acquire a function. A large part of it (or even all of it) may not do so and may be eliminated only on an evolutionary time scale. Meanwhile, new DNA of the same and similar kind may continue to be produced so that at a given point of time there will always be large amounts of non-specific DNA. This fraction is best described as ‘incidental’ rather than ‘selfish’ DNA. We may call it incidental because it is a byproduct of the inherent property of mutability of the genome, a characteristic to which natural selection attaches great importance even if it leads to the production of repeated sequences and a wasteful deployment of energy. Viewed in this light, non-functional DNA is very much a product of natural selection — a selection operating for mutability per se. Its relative abundance is probably a function of its nonfunctional nature for any other DNA which carries information of one kind or another would create genetic imbalance and would be quickly rejected.
…
Nature places considerable premium on playing safe so that it will not run short of raw material even if this means indiscriminate production leading to sequences which are destined to remain functionless.
Now, Dr. Musso may interpret this very differently, but I take it to mean that Jain argued that non-coding DNA was preserved by natural selection specifically because it may become useful as a source of new genes. Moreover, this would have to be non-coding DNA that was preserved in this way because adding coding regions for future use would create complications in genic function. I have discussed in various posts (e.g. here, here) why this notion is untenable.
UPDATE: My interpretation of Jain (1980) was that he was arguing that non-coding DNA is preserved by selection because it contributes to mutability. Further discussion with Jonathan Badger, and another re-read of Jain (1980) in the context of alternative interpretation, has bolstered the conclusion that he was in fact suggesting something different from what I said. The much more reasonable interpretation, and what I now think he was actually arguing, is that the genome is inherently unstable for reasons unrelated to non-coding DNA and that this is maintained by selection (though, it must be said, not in the usual sense but interlineage level) and the accumulation of non-coding DNA is a byproduct of this. I will accept that the authors of the paper that began the discussions saw it this way — though their phrasing “IF does exist a mechanism for genome size increase, THEN maybe the resulting long-term advantage can overcome the short-term disadvantage” is easily confused with arguing that non-coding DNA generates some long-term advantage that overcomes its immediate disadvantage (rather than representing a side-effect of some other process with a long-term advantage). And then, there is still the issue of what the original article stated:
From this point of view, we can think of TMs in our simulations as organisms trying to increase their gene pools adding new genes assembled from junk DNA. If the organisms possess more junk DNA it is possible to test more “potential genes” until a good one is found.
Though I doubt he will read this post, I do apologize to Dr. Jain if indeed I misinterpreted his argument. That said, I do think his phrasing of selection is imprecise and that this probably contributed to the confusion. In my original citation written 8 years ago, I cited Jain as an example of a “noncoding DNA is there because it might be useful” line of thinking, and while he may have been an inappropriate example, this notion is still around and needs to be fixed. In any case, I have not changed my opinion that the article that started this discussion drew undue links between a model and biological genome evolution, and that their results have little bearing on the genome size question.
________
Update, part two
I hate to keep updating this post (though I have preserved the original form with strikeouts), but I just knew I was not the only person to have interpreted Jain (1980) as suggesting that noncoding DNA was preserved because of its potential long-term benefits. It seems W.F. Doolittle (an originator of the “selfish DNA” idea, and whose paper Jain was commenting on) got the same impression. I will quote at length from Doolittle (1982), in which he discussed the varying reactions to the notion of selfish DNA shortly after it was proposed (italics in original, most in-line references omitted).
(c) The long-term evolutionary advantage of genomic rearrangements. Transposable elements promote genetic rearrangements, and the kinds of rearrangements (transpositions, deletions and inversions) seem similar in both prokaryotes and eukaryotes. This (and the occasional turning on and off of genes adjacent to the site of insertion) appears to be all that many, perhaps most, transposable elements actually do for the organism which bears them and it does not seem to be a good thing. Selection operating on individuals should eliminate such elements. Thus many have claimed that transposable elements are maintained because they play important “evolutionary roles”. This is not a straw man which Carmen Sapienza and I set up in order to have a hypothesis against which to pit the notion of selfish DNA. I can only document this with quotations not, I hope, taken out of context:
“Whether they (insertion sequences) exert functions at these positions or are simply kept in reserve as prefabricated units for the evolution of new control circuits remains unclear.”
“It is possible that the sole function of these elements is to promote genetic variability…”
“A tenable hypothesis regarding the function of transposition is that it allows adaptation of a particular cell to a new environment.”
“All these alterations could lead to changes in structural gene function and in the control of gene expression and could provide organisms with a means of rapid adaptation to environmental change.”
Evolutionary roles have similarly been invoked for heterochromatic highly repetitive DNAs, whose presence does affect recombination in neighbouring and distant regions and whose characteristics may (although the experimental evidence is not strong) affect chromosome pairing.
Neither we [Doolittle and Sapienza] nor Drs Orgel and Crick denied that transposable elements or heterochromatic highly repetitive DNAs have such evolutionary effects, nor that these effects might not be important, perhaps even as the basis for macroevolutionary change. What we were arguing against was the assumption that these elements arose through and are maintained by natural selection because of these effects.
This assumption is often only implicit in the writings of many who suggest that the only roles of mobile dispersed and tandemly reiterated DNAs are evolutionary ones. Thus we have been accused by some of these of misrepresenting their positions and thus indeed of attacking straw men after all. I apologize to those who feel we have put words in their mouths. But I do not see how statements that the only “functions” of transposable elements or highly repetitive DNAs are to generate or modulate genetic variability can mean anything other than that natural selection maintains, and probably even gave rise to, such elements through selection for such “functions”. Shapiro (1980) has been brave enough to articulate this view outright:“Why, then, are insertion elements not removed from the genome? I think the answer must be that there is a selective advantage in the ability to generate new chromosome primary structure.”
Those who speculate on the function of excess DNA have formulated this position in a more extreme way. For instance, Jain (1980) states
“at a given point of time there will always be large amounts of non-specific DNA. This fraction is best described as ‘incidental’ rather than ‘selfish’ DNA. We may call it incidental because it is a byproduct of the inherent property of mutability of the genome, a characteristic to which natural selection attaches great importance even if it leads to the production of repeated sequences and a wasteful deployment of energy. Viewed in this light, non-functional DNA is very much a product of natural selection — a selection operating for mutability per se.“
The question of whether natural selection operates in this way, that is of whether the evolutionary process itself evolves under the direct influence of natural selection, lies at the root of the real controversy over whether self-maintaining, structured, genomic components without phenotypic function can properly be called “selfish”. This may seem like a small and metascientific quibble. In fact it is not; it is one of the most troublesome questions in evolutionary biology today. It manifests itself in debates over the origin and maintenance of mechanisms involved in the optimization of mutation rates, recombination, sexual reproduction, altruistic behaviours of all sorts and even speciation. Such mechanisms are not clearly advantageous to, and can be detrimental to, the fitness of the individual. Yet they may increase the long-term survival properties of the group to which the individual belongs, thus seeming to be the product of what has been called “group selection”.
________
Doolittle, W.F. (1982). Selfish DNA after fourteen months. In: Genome Evolution (G.A. Dover and R.B. Flavell, eds.), Academic Press, New York, pp.3-28.
Jain, H.K. (1980). Incidental DNA. Nature 288: 647-648.
I recall early on that I made a special post expressing excitement that Genomicron had received 1,000 hits. I am hopeful that this announcement will be similarly quaint in the not too distant future. It seems that as of this morning, Genomicron has 300 subscribers (well, 301, but one of them is me). If this continues, we may need a term for Genomicron readers — please note that I am prepared to veto “Genomicronies”. Thank you to everyone who has been reading, and don’t forget to tell your friends and colleagues to check it out.
In a follow up to my last post about funny lines, here are some more funny lines.
Some of these are borrowed from comedians (though I don’t remember who), and quite a few are, I think, original (by me or my brother). If you want to double check, feel free to do so. If you don’t find them attributed to anyone else, you can link to this list. 😀
Over on Sandwalk, Larry reposts a list of euphemisms for stupidity (“Not the sharpest knife in the drawer”, “One neuron short of a synapse”, so on).
There are some on the list that are biological, but I think we could benefit from more. I will start things off with one of my own:
He’s not the brightest bioluminescent bacterium in the photophore.
Go.
___________
Addendum:
For some reason, one that my brother sometimes says (with a requisite straight face) cracks me up:
He’s not the smartest guy in the world, if you know what I’m saying.
Some of you may remember the post from Dec. 1, 2007, on Genome size, code bloat, and proof-by-analogy (which was posted on DNA and Diversity also). This post referred to a computer study published in the online, non-peer-reviewed arXiv database by Feverati and Musso (2007). Recently, Dr. Musso has been kind enough to provide some responses to my post, though of course very few people will notice because they are located within the comments section of a post that is more than two months old. So, I reprint them here in full, with my responses interspersed throughout.
As an author of the article discussed in this blog I would like to reply to Prof. Gregory criticisms. First of all I think that after writing such an harsh comment on an article, it would be a matter of good taste to inform the authors just to give them the opportunity to reply (that does not cost a great effort since email addresses are in the paper). I stumbled in this review by chance and only recently, and so my answer comes a bit late.
Fair enough (and my apologies if this caused frustration), though it was not my intent to enter into a discussion about the paper, only to post my thoughts and move on. In particular, I had been asked by a reporter for my thoughts about this paper — in the context of understanding genome size — and instead of sending an email I decided to post them.
Even if Prof. Gregory introduces our article saying that: “the authors ….decided that a computer model could provide substantive information about how genomes evolve in nature”, actually we never said that. We have a brief subsection in the conclusions (less than half a page long) where we comment on the biological relevance of our results. Such subsection begins with the following words: “In this section we put forward some biological speculations inspired by our model”. It seems to me that “biological speculations” is quite different from “substantive information”; moreover we speak only of possible advantages in terms of “evolvability”, and that’s also very
different from saying “how genomes evolve in nature”.
Allow me to insert the abstract of the paper:
The development of a large non-coding fraction in eukaryotic DNA and the phenomenon of the code-bloat in the field of evolutionary computations show a striking similarity. This seems to suggest that (in the presence of mechanisms of code growth) the evolution of a complex code can’t be attained without maintaining a large inactive fraction. To test this hypothesis we performed computer simulations of an evolutionary toy model for Turing machines, studying the relations among fitness and coding/non-coding ratio while varying mutation and code growth rates. The results suggest that, in our model, having a large reservoir of non-coding states constitutes a great (long term) evolutionary advantage.
Furthermore, the first two paragraphs of the paper, and the last two (about 1/4 or more of the entire discussion and conclusion), are about genome size, and I believe that one could be forgiven for interpreting this as indicating that the authors saw a strong connection between their study and genome size evolution.
Prof. Gregory next discusses the validity of our assumptions. First of all I would like to notice that since we wrote:”For the sake of simplicity, we imposed various restrictions on our model that can be relinquished to make the model more realistic from a biological point of view”, it means that we are fully aware that our assumptions are NOT realistic. So I can’t understand what’s the point in putting such emphasis in explaining the reasons why they are not. A much briefer comment would have been: “as the authors candidly admit, their assumptions are unrealistic”.
I am glad we are in agreement that the assumptions are unrealistic. The reason I emphasized this so strongly is that this is a blog about genomes and evolution that is meant to provide information to readers with a diversity of educational backgrounds. Dr. Musso and I may know that these assumptions are very unrealistic, but many readers would not. More than a critique of this paper, I was providing details about how evolution actually operates in nature. Incidentally, these criticisms regarding the unrealistic assumptions are the same ones I would have made had I been reviewing this article for a peer-reviewed journal — at least, if any connection was attempted between this model and genome size in eukaryotes.
I would like to stress that a “model” is a simplified version of reality, while a “toy model” is oversimplified to the point that the model is just a caricature of the reality. Still toy models are precious instruments in the investigation of complex systems, and can give some hints and help comprehension on the modelized phenomenon. First example that comes to my mind is the “HPP lattice gas model” for hydrodynamics. Imposing the level of detail requested by prof. Gregory would result not in a toy model and neither in a model but in an accurate description of reality (admitting that by now we have a perfect understanding of all biological phenomena). Moreover with such level of detail it would have been impossible to reach our aim (measuring the optimal coding/non-coding ratio in our model), partly for the computational time required and partly for the impossibility to interpret unambiguously the results obtained.
I think we are in agreement on this, though my conclusion is that if a model has too be too simple to reflect reality then it is not useful, whereas Dr. Musso seems to be saying that because only simplified models can be used, they are justified. The notion that biological evolution is similar to hydrodynamics, and indeed this view of models generally, is the reason for my original post. I noted in the original post that their model may have been the greatest of its sort ever developed, but that it has no bearing on biological evolution — if we agree that it is unrealistic, then why begin and end a paper with a multi-paragraph discussion of a biological phenomenon?
I would like to stress that since, in our model, adding a new state has a NEUTRAL impact on the fitness, the process of state-increasing is, by definition, NON-adaptative. I agree with prof. Gregory that it would have been better to use “mimic Darwinian evolution” instead of “mimic biological evolution”, but I have also a provocative question: was Darwin’s theory to be rejected as a theory of biological evolution since he did not specify the exact mechanisms of mutation?
As a matter of fact, Darwin’s theory of natural selection (but not the fact of evolution) was not widely accepted in his own time in part because he lacked a basis for inheritance, and it was largely rejected in the early 1900s, in part because new knowledge about heredity (namely the rediscovery of Mendelian inheritance) seemed to contradict its assumptions. In any case, I don’t really see what the relevance of this well known history is to the discussion of these models.
In its conclusion prof. Gregory suggests that we claim that “Non-coding DNA does accumulate “so that” it will result in longer-term evolutionary advantage”. We ABSOLUTELY NEVER stated such a non-sense.
If I may quote once more from the article:
In this section we put forward some biological speculations inspired by our model. There are two way [sic] of identifying TMs [Turing machines] with biological entities and they suggest two ways up to which the accumulation of non-coding free to mutate DNA can play a role for “evolvability”. In the first one we identify TMs with organisms and coding-states with genes. We have to stress that the mechanism of transcription is different in the two contexts. For TMs transcription is serial, so that states must be transcribed, one at a time, in prescribed order, while in biological organisms transcription of genes can happen in parallel. We can interpret TMs states as genes accomplishing both a structural and regulatory function, since a coding state both affects the output tape and specifies which state has to be successively transcribed. From this point of view, we can think of TMs in our simulations as organisms trying to increase their gene pools adding new genes assembled from junk DNA. If the organisms possess more junk DNA it is possible to test more “potential genes” until a good one is found.
I may have misinterpreted what the authors meant by this, but it seems to imply that junk DNA serves as a reservoir of potential genes and that this increases evolvability. The implication drawn by many authors, including some biologists like Collins, is that this is why junk is there (“It is not the sort of clutter that you get rid of without consequences because you might need it. Evolution may need it,” [Collins] said.”). Either way, this served as a useful launching pad to reiterate the important point that this makes no sense evolutionarily if framed as a cause of junk DNA rather than as a potential consequence.
It is curious that the same accuse was moved by prof. Gregory in its article “Coincidence, coevolution, or causation? DNA content, cell size, and the C-value enigma”, that we cite in our paper, to an article by Jain that we also cite in our paper. So, either prof. Gregory has a very poor opinion of our intelligence, or he thinks that we do not read the articles that we cite.
I reject the dichotomy presented there. Some other possibilities, inter alia, are that the authors did not interpret the papers the same way as I did, or they read mine by disagreed with my argument, or they partially misunderstand how evolution occurs. Given that even some biologists who work on real-life genomes make this mistake, I hardly think this implies a lack of intelligence, only a lack of background.
Let us state, unambiguously, what we and Jain really say: “IF does exist a mechanism for genome size increase, THEN maybe the resulting long-term advantage can overcome the short-term disadvantage” (Jain was referring to the selfish dna as the genome increasing mechanism while we do not give any preference). Prof. Gregory reverts the implication: “IF there is a long-term advantage THEN the mechanism of genome increase is the product of selection”, and then explains us that it can’t be true. Incidentally, in the case of Jain, I think that what he was really intending can be clearly understood just by the title: “Incidental DNA”.
“Long-term advantage” and “short-term disadvantage” imply selection, and there does not seem to be much difference between the two ways of stating this. Moreover, as I noted in my original post and in more detail in an earlier post, long-term inter-lineage selection can potentially overcome short-term disadvantage, but this is not why non-coding DNA exists in the first place. If Dr. Musso and others understand it that way, then so much the better. But many people do not, and so taking an opportunity to clarify the issue once more was worthwhile.
Finally, let us state, very very briefly what in our paper we really did. We built up an abstract evolutionary model with mechanisms of mutation and genome increase, in such a way that we could exactly measure what is, in our model, the coding/non-coding ratio, and we found that it can’t be more than 2%. We were thinking that such result could be interesting also for biologists, maybe we were wrong.
Once again, this strongly indicates that Dr. Musso sees his “evolutionary model with mechanisms of mutation and genome increase” as a way of studying real biological genome size evolution, which was the entire reason for the post in the first place.
Biologists may indeed have an interest — I suggest that the paper be submitted to a peer-reviewed biological journal.