tag:blogger.com,1999:blog-37148773.comments2024-03-19T00:24:23.577-04:00<center>Sandwalk</center>Larry Moranhttp://www.blogger.com/profile/05756598746605455848noreply@blogger.comBlogger103601125tag:blogger.com,1999:blog-37148773.post-36380446116132194282024-03-19T00:24:23.577-04:002024-03-19T00:24:23.577-04:00@Larry: Joe, what do you personally think about a...@Larry: <em>Joe, what do you personally think about all the morphological variation we see in humans today? Do you think it's all either slightly beneficial or slightly deleterious?<br /><br />Do you think that all of the morphological differences between African and Asian elephants are due to selection for beneficial traits in different environments? Could some of them (e.g. larger ears) be effectively neutral?</em><br /><br />Not plausibly. If the effective population size of elephants was, say, 1,000,000 over the last millions of years, then the "drift barrier" is approximately <em>|s| > 1/4,000,000</em>. To have drift have much effect, you need to have selection coefficient less than that. Plausible? Not very. Especially since changes in morphological and behavioral characters such as ear size are correlated with other traits. The spandrels criticism is valid, not because neutral mutation overwhelms selection, but because selection on correlated traits is important.<br /><br />Of course, selection on molecular substitutions can be much weaker.Joe Felsensteinhttps://www.blogger.com/profile/06359126552631140000noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-21773581354772507062024-03-18T09:58:09.828-04:002024-03-18T09:58:09.828-04:00@apalazzo: I agree. It's frustrating to see ho...@apalazzo: I agree. It's frustrating to see how Philip Ball gets himself all tied up in knots. He seems to be arguing that our nice neat orderly view of biology is flawed because it's really much more complicated than that. You and I agree that biology is messy and we reject the strawman version of biology that he sets up. <br /><br />Ball interprets the data differently. His logic is often inconsistent but he usually interprets the complications to be signs that there's something mysterious going on behind the scenes. Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-46065794307505510442024-03-18T09:49:58.333-04:002024-03-18T09:49:58.333-04:00@SPARC: Thank-you for spotting that error. I fixed...@SPARC: Thank-you for spotting that error. I fixed it.Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-47200955074099510562024-03-18T07:26:04.999-04:002024-03-18T07:26:04.999-04:00I'm part way through the book as well and I...I'm part way through the book as well and I'm equally frustrated. There are quite a few strawman arguments and non sequiturs. The thing that is angering me is how he first states that different fields have different definitions of “gene”, but if you use the antiquate Mendelian definition, biology doesn’t make sense, so we should thus throw out the concept of genes. What he fails to mention, is the molecular definition is fine and that we CAN make sense of much of biology if we stick to this. What we need to throw out are the other definitions of genes, which do no make much sense and fail to give insight into what is going on. DUH.<br /><br />Over and over he does this. He brings up different “views”, claims its all chaos, and then advocates that we should just throw everything out. SO DUMB.apalazzohttps://www.blogger.com/profile/06077383161556651420noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-17018533085290487662024-03-18T02:47:10.168-04:002024-03-18T02:47:10.168-04:00If the binding would be as specific and exclusive ...If the binding would be as specific and exclusive as Walter and others assume I wonder if they are unaware that EMSAs and footprinting experiments which employ nuclear extracts necessitate the addition of unspecific competitor nucleic acids to reduce unspecific binding of proteins for which the labeled DNA doesn't contain any binding sites. Maybe they just do in vivo cross-linking which just tells you that a protein was bound to the DNA but not if the binding was specific.<br />SPARChttps://www.blogger.com/profile/09563722742249547887noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-8559095455993576302024-03-18T02:03:16.041-04:002024-03-18T02:03:16.041-04:00It should be Fick’s rather than Frick’s law.It should be Fick’s rather than Frick’s law.SPARChttps://www.blogger.com/profile/09563722742249547887noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-81757174361632244382024-03-17T10:52:59.248-04:002024-03-17T10:52:59.248-04:00@gert korthof: Yes, there is much, much more wrong...@gert korthof: Yes, there is much, much more wrong with Philip Ball's book. I'm preparing multiple posts. <br /><br />I do not recommend his book. If you can't see what's wrong with it you should not be reading it. Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-11602201616342973842024-03-17T04:38:54.664-04:002024-03-17T04:38:54.664-04:00and there is much, much more wrong with Ball's...and there is much, much more wrong with Ball's book...gert korthofhttps://www.blogger.com/profile/02176669976311883850noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-2166584206005534452024-03-16T21:02:38.603-04:002024-03-16T21:02:38.603-04:00I'm intrigued by you referring to Einstein sim...I'm intrigued by you referring to Einstein simply as "Albert" in your first note.<br />-CésarAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-75310289943458056772024-03-16T20:52:54.003-04:002024-03-16T20:52:54.003-04:00You describe an odd situation in which selection i...You describe an odd situation in which selection is powerful enough to fix an adaptive bit of sequence but not enough to preserve its sequence. I'm not sure that needs refutation.John Harshmanhttps://www.blogger.com/profile/04478895397136729867noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-65630002995387341182024-03-16T17:35:48.566-04:002024-03-16T17:35:48.566-04:00Add another book to the pile.
Thanks for the rec...Add another book to the pile. <br /><br />Thanks for the rec.Rarian Rakistahttps://www.blogger.com/profile/07386271335254334657noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-89687231491533596442024-03-16T17:29:08.287-04:002024-03-16T17:29:08.287-04:00We would expect sequences that functioned against ...We would expect sequences that functioned against severe pathogens, and/or more frequently encountered pathogens, to be more conserved than sequences that functioned against less severe pathogens, and/or encountered pathogens less frequently. Thus, some sequences would have come under selection a mere several generations before the current generation, and some others, hundreds, or perhaps thousands of generations before the current generation. Present evidence on this, and you might well discover a fatal flaw in this particular anti-junk argument.<br /><br />forsdykenoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-78887910224174724752024-03-16T17:08:47.369-04:002024-03-16T17:08:47.369-04:00Donald Forsdyke: The fatal flaw in this explanatio...Donald Forsdyke: The fatal flaw in this explanation is that we would expect the sequences in question to be conserved, so nobody would consider them junk DNA. Since the great bulk of human sequences (~90%) isn't conserved, we would not expect to find these "RNA antibodies" or other sequences involved in the proposed pathogen response there. Nor, for similar reasons, can it explain the differences in genome size among species.John Harshmanhttps://www.blogger.com/profile/04478895397136729867noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-74636618030093249482024-03-16T12:08:24.795-04:002024-03-16T12:08:24.795-04:00RECONCILIATION
Nils Walter suggests that differen...<b>RECONCILIATION</b><br /><br />Nils Walter suggests that different scientific fields view the “junk” hypothesis differently (“two different scientific fields, which he usually identifies as geneticists and evolutionary biologists versus biochemists and molecular biologists”). Having for six decades worked in these fields (plus immunology), I again draw attention to the possibility that certain sequences do not operate in every generation but may only function in occasional generations.<br /> <br />If an RNA sequence happens to complement the sequence of an intracellular pathogen, then a length of dsRNA will form that may activate various alarms (e.g. inhibit protein synthesis). This was discovered in the early 1970s by various biochemists associated with the Korner laboratory (Cambridge). Even if operating rarely, if that operation is advantageous the sequence can still be conserved by natural selection. Here is one of my past Sandwalk comments that draws attention to Zabolotneva’s work on the topic:<br /><br /><b>INFECTION TRIGGERS PERVASIVE TRANSCRIPTION</b><br /><br />A viral infection is a stress, and stress has long been known to provoke the transcription of repetitive elements (e.g. Alu; Liu et al, 1995), from which run-on transcription can extend into neighboring regions of “junk” DNA (Cristillo et al. 1991). <br /><br />Thus, we and others (e.g. Zabolotneva et al. 2010) have suggested an RNA-based "intracellular 'immune system'," where alarms begin ringing when an RNA of viral origin forms dsRNA with an 'RNA antibody' of host origin. Like us, Zabolotneva et al. suspect that this may explain the variable quantities of 'junk DNA' found in genomes:<br /><br />Quote:"Casual [random] combinations of nucleotides in ... the genome might create new DNA motifs that theoretically, after being transcribed, could be used by the host organism as a tool for recognition and targeting of intracellular pathogen transcripts. Novel transcribed [host] DNA motifs that would target the host genes [i.e. 'self'] would be eliminated from the genome [negative selection], whereas those that complementarily match the pathogen RNAs would be positively selected. Neutral motifs [yet to find a pathogen target but not interacting with 'self'] could be 'stored' in the genomes as ordinary non-coding DNA." <br /><br />Others envisage a “retroposon transcriptome” (Faulkner et al. 2009).<br /><br /><br /><b>References</b><br /><br />Cristillo et al. (2001) Double-stranded RNA as a not-self alarm signal: to evade, most viruses purine-load their RNAs, but some (HTLV-1, Epstein-Barr) pyrimidine-load. J. Theor. Biol. 208, 475-491.<br /><br />Faulker et al. (2009) The regulated retroposon transcriptome of mammalian cells. Nature Genetics 41, 563-571.<br /><br />Liu et al. (1995) Cell stress and translational inhibitors transiently increase the abundance of mammalian SINE transcripts. Nucleic Acids Res. 23, 1758-1765. <br /><br />Zabolotneva et al. (2010) How many antiviral small interfering RNAs may be encoded by the mammalian genome? Biology Direct 5, 62.Forsdykehttps://www.queensu.ca/academia/forsdyke/noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-61612696393657686242024-03-14T11:10:29.991-04:002024-03-14T11:10:29.991-04:00@SPARC: I struggle to understand the worldview of ...@SPARC: I struggle to understand the worldview of the anti-junk crowd. It's seems to me that they have convinced themselves that human (and mouse?) cells are incredibly complex so there must be lots and lots of regulatory sequences, regulatory RNAs, ubiquitous alternative splicing, mysterious functioning transposon fragments, and a complex network of chromatin interactions. All of this is mediated by the dark genome that's full of mysterious undiscovered function.<br /><br />Normally you would look for evidence to support such a worldview and accept all the nasty little facts that conflict with your hypothesis. That doesn't seem to be happening in this case. Instead, the anti-junk crowd is determined to come up with more and more weird ad hoc excuses to explain away evidence that contradicts their views. Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-8095300151849331772024-03-14T02:58:53.116-04:002024-03-14T02:58:53.116-04:00If cells are as complex as Walter assumes and all ...If cells are as complex as Walter assumes and all the non-intronic non-coding spurious RNAs were functional and of such regulatory importance then why don't they show up in mouse ENU screens at the same frequencies as mutations in protein coding genes (mutated introns show up more frequently because mis-splicing may interfere with protein expression). <br />The same is true for gene trap analyses in murine ES cells. For a gene traps to work they just have to be inserted in any kind of transcribed sequence. This approach will only address sequences transcribed in ES cells. However, the only counter argument would be that non-coding RNAs don't play a role in the regulation of ES cells which would be quite a stretch giving the fact that the no-junk proponents often argue that these sequences especially function during development. In addition, if a piece of DNA is only transcribed once in a while in one of thousands cells a gene trap will not work and renders these trapped sequence junk.<br /> SPARChttps://www.blogger.com/profile/09563722742249547887noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-25108710341442174962024-03-12T21:39:07.527-04:002024-03-12T21:39:07.527-04:00Are there many current evolutionary biologists who...<i>Are there many current evolutionary biologists who publish papers defending the idea that the definition of evolution is restricted to changes in morphology and/or behavior?<br /><br />Are there any experts in population genetics who make such a claim?</i><br /><br />Current? Perhaps not. But Ernst Mayr used to make that claim.John Harshmanhttps://www.blogger.com/profile/04478895397136729867noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-81472256790545611782024-03-12T17:47:01.944-04:002024-03-12T17:47:01.944-04:00Joe Felsenstein says, "Some of the miscommuni...Joe Felsenstein says, "Some of the miscommunication involves the phrase "amount of evolution", which is ambiguous as to whether it counts all changes in sequences, or only changes that affect morphology and/or behavior."<br /><br />Are there many current evolutionary biologists who publish papers defending the idea that the definition of evolution is restricted to changes in morphology and/or behavior?<br /><br />Are there any experts in population genetics who make such a claim? <br /><br />Joe, what do you personally think about all the morphological variation we see in humans today? Do you think it's all either slightly beneficial or slightly deleterious? <br /><br />Do you think that all of the morphological differences between African and Asian elephants are due to selection for beneficial traits in different environments? Could some of them (e.g. larger ears) be effectively neutral?Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-57566490204453280612024-03-12T17:31:36.985-04:002024-03-12T17:31:36.985-04:00@Joe Felsenstein says, "Anyone want to argue ...@Joe Felsenstein says, "Anyone want to argue that the elephant's trunk gets longer and shorter mostly by neutral mutation and genetic drift? I get the impression that Larry does."<br /><br />Really? Why in the world world you say that?Larry Moranhttps://www.blogger.com/profile/05756598746605455848noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-74563767827416131452024-03-12T01:51:21.373-04:002024-03-12T01:51:21.373-04:00One guy says "look at how many mutations fix ...<em>One guy says "look at how many mutations fix are neutral, it's almost all of them", and then another guy points at some highly adaptive morphological character and says "clearly selection is most important." I always get the sense they're talking past each other.</em><br /><br />They are. Given the large amount of junk DNA, most mutants that fix are of course neutral. But that does not establish that mutations in coding sequences or control regions that affect morphology (for example) can be assumed to be neutral. Some of the miscommunication involves the phrase "amount of evolution", which is ambiguous as to whether it counts all changes in sequences, or only changes that affect morphology and/or behavior.<br /><br />Joe Felsensteinhttps://www.blogger.com/profile/06359126552631140000noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-87794882168491780542024-03-12T00:56:27.475-04:002024-03-12T00:56:27.475-04:00@Joe Felsenstein
Visible change in morphological c...@Joe Felsenstein<br /><em>Visible change in morphological characters almost always has enough fitness effect that pure neutrality is not very plausible. Anyone want to argue that the elephant's trunk gets longer and shorter mostly by neutral mutation and genetic drift? I get the impression that Larry does.</em><br /><br />Alot of this "how important is selection vs drift" debates often seems to reduce to something like that. One guy says "look at how many mutations fix are neutral, it's almost all of them", and then another guy points at some highly adaptive morphological character and says "clearly selection is most important." I always get the sense they're talking past each other. Mikkel Rumraket Rasmussenhttps://www.blogger.com/profile/07670550711237457368noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-21168387082257060542024-03-12T00:04:04.314-04:002024-03-12T00:04:04.314-04:00I argued that when Zuckerkandl and Pauling propose...I argued that when Zuckerkandl and Pauling proposed the molecular clock they thought that constant selection explained it, not neutral evolution.<br />Morgan, G. J. (1998). Emile Zuckerkandl, Linus Pauling, and the molecular evolutionary clock, 1959-1965. Journal of the History of Biology, 155-178.<br />https://www.researchgate.net/profile/Gregory-Morgan-2/publication/226242136_Emile_Zuckerkandl_Linus_Pauling_and_the_Molecular_Evolutionary_Clock_1959-1965/links/54d558070cf25013d02b025a/Emile-Zuckerkandl-Linus-Pauling-and-the-Molecular-Evolutionary-Clock-1959-1965.pdfGregory Morgannoreply@blogger.comtag:blogger.com,1999:blog-37148773.post-53335001535942050252024-03-11T16:59:22.851-04:002024-03-11T16:59:22.851-04:00The Gould and Lewontin "spandrels" paper...The Gould and Lewontin "spandrels" paper was not just raising the possibility of neutral mutation. It was asking whether, when you saw changes that looked like natural selection, could you conclude that your particular selection hypothesis was correct. You could not assume that, but not just because neutral change was possible. It could be that the change you saw in morphological characters was not due to selection on those characters, but selection on other characters that were genetically correlated with them.<br /><br />Spandrels in cathedrals were quite deliberately put there by architects -- they weren't neutral, without them the dome would fall down. We are not justified in assuming that they are there to have a place to draw pictures of saints.<br /><br />Visible change in morphological characters almost always has enough fitness effect that pure neutrality is not very plausible. Anyone want to argue that the elephant's trunk gets longer and shorter mostly by neutral mutation and genetic drift? I get the impression that Larry does.Joe Felsensteinhttps://www.blogger.com/profile/06359126552631140000noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-5167701421832646652024-03-11T13:43:29.409-04:002024-03-11T13:43:29.409-04:00From the point of view of molecular phylogenetics,...From the point of view of molecular phylogenetics, we would prefer that all sequences be evolving neutrally. It makes the models used in evaluating trees more tractable, it minimizes problems of systematic convergence, and it provides the most phylogenetic signal per unit time.John Harshmanhttps://www.blogger.com/profile/04478895397136729867noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-65289114163083924492024-03-11T11:29:03.304-04:002024-03-11T11:29:03.304-04:00Thank you. I read the Galtier paper and this post ...Thank you. I read the Galtier paper and this post putting it in context makes me think I understand it a bit better.Don Catesnoreply@blogger.com