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Antievolution.org Discussion Board > From the Panda's Thumb > After the Bar Closes... > Evolution of the horse; a problem for Darwinism?

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JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 13 2007,17:22    Quote (Daniel Smith @ Oct. 13 2007,14:58)     Quote (JAM @ Oct. 13 2007,13:49) Maybe while you're trying to wrap your head around linkage disequilibrium, you can point us to a designed mechanism involving large numbers of similar, but not identical, parts, that have only partially overlapping functions. That mechanism would be analogous to living ones. So we're accepting analogies as evidence now? No, I'm pointing out that the analogy you're offering as evidence is simply wrong.     Quote Quote Also, you can directly test your hypothesis that noncoding regions are conserved by peeking at the VISTA genome browser: http://pipeline.lbl.gov/cgi-bin/gateway2?bg=hg16 You're not gonna like what you see, so you probably should blow it off and not try to grapple with any real evidence. Here's an idea--pretend that our calling you out on your false claims is mean, which automatically makes your false claims correct (at least in your mind). I went to the vista site, but I'm not sure how to use it.  I'll have to read the help file I guess. I suggest clicking the "Go" button to begin.   Quote BTW, you are generally mean - but I'm still here. Your meanness has nothing to do with your rightness. Good for you. I have to admit, though, that I tend to be more mean when I'm right, particularly when dumping evidence on someone as arrogant as you, who pretends to have a better understanding of my life's work than I do. Or someone who claims to have examined evidence, but moves the goalposts to someone else's "descriptions" when challenged. Do you get a feeling for my perspective?

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 13 2007,17:33    Daniel, Here's a good VISTA example: http://pipeline.lbl.gov/servlet....llbar=0 This is mouse against human, dog, rat, and chicken in graphs 1-4 respectively.

mitschlag Posts: 236 Joined: Sep. 2006 (Permalink) Posted: Oct. 13 2007,18:22    Quote (Daniel Smith @ Oct. 13 2007,13:53)   Quote (mitschlag @ Oct. 10 2007,12:47)       Quote (Daniel Smith @ Oct. 10 2007,02:30) The results that would falsify my hypothesis would be if the coding sequences showed evolutionary constraint while the non-coding sequences didn't. There's a fair amount of evidence showing that (contrary to expectation) non-coding sequences have fewer base changes than coding sequences, see, for example: http://www.biomedcentral.com/1471-2148/7/66         Quote The primary result is that the mean rate of intergenic nucleotide substitution is two-thirds that of the synonymous coding data, with an absolute rate estimated to be 1.05 × 10-8 substitutions per site per year. This result holds with alternative nucleotide models (see Methods), and thus does not appear to be solely an issue of estimation procedures. Slower rates in non-coding regions relative to synonymous sites are becoming a surprisingly frequent observation. For example, a recent study of Drosophila demonstrated that non-coding DNA evolves considerably slower than synonymous sites in terms of both divergence between species and polymorphism within species [16]. By comparing studies, one can also make the case that pseudogenes [32,33] and introns [34,35] evolve more slowly than synonymous sites in apes and other mammals [13,36-38]. Studies of mammalian intergenic regions have also found slower rates than synonymous sites [35,39,40]. Although most of these studies encompass only a handful of genes, an overall picture of relatively slow non-coding rates is emerging. What do you make of that? If this is true, then it would be a confirmation of my hypothesis with better than expected results. It's true, all right, but it doesn't confirm your hypothesis. To learn why, read the cited paper.  Hint: TE=transposable element. (Sorry that I won't be able to participate in this discussion for the next two weeks due to travel in arcane regions.  In the meantime, I want to commend DS for  his courteous and patient responses to the many challenges that have been addressed to him.) -------------- "You can establish any “rule” you like if you start with the rule and then interpret the evidence accordingly." - George Gaylord Simpson (1902-1984)

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 13 2007,23:01    Quote (jeannot @ Oct. 13 2007,15:16) So what about the fact that mutation rates are far higher at synonymous sites? As I understand it (and I just learned this) synonymous sites are sites that will accept a substitution with no functional change.  Therefore, there's no reason that these sites wouldn't show higher mutation rates.  The question is: why do sites that are supposedly non-functional show more constraint than synonymous sites? -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 13 2007,23:32    Quote (JAM @ Oct. 13 2007,17:14)     Quote (Daniel Smith @ Oct. 13 2007,14:00)       Quote (JAM @ Oct. 10 2007,10:40) Here's an opposing hypothesis: Known functional sequences will be evolutionarily conserved. Most sequences will not be conserved. We will continue to find functions for some conserved sequences for which no function has been identified. What do you think? Shall we look at the evidence to see which hypothesis is better supported? Yes, let's look.  But be warned, I'll be approaching the evidence from a different perspective than you and won't accept any preconceived ideas as part of the interpretation. Daniel, this is why real, honest scientists make predictions BEFORE they get the data. My hypothesis predicts that when we graph position on the x axis and % identity on the Y axis, we will see this, with the high points representing conserved sequences, which include, but are definitely not limited to, protein-coding sequences: /\_/\___ Your hypothesis predicts that we will see a flat line wherever we look: -------------- My hypothesis does not predict a flat line - except within a lineage.  By "lineage" I mean either the same species or very closely related species.  As an example I would think something along the lines of the African vs. Asian elephant.  This is why I said that the test needs to be done within the lineage to test my hypothesis.   Quote     Quote What I mean is that the perceived "rate of mutation" is often calculated by a comparison of species that are assumed to have evolved from a common ancestor via an accumulation of random mutations. Not even remotely close, Daniel. Mutation rates are much more directly measured by quantitating new mutations; for example, we can measure the rate of new cases of autosomal dominant diseases that aren't inherited from parents. No assumptions are necessary to distinguish between our hypotheses. We are simply looking at differences between lineages for orthologous regions of the genome. But orthologous regions are regions that are thought to be homologous due to speciation - which is assumed to have occurred by an accumulation of mutations - isn't that correct?   Quote     Quote Since I am opposing that theory, I won't accept that assumption. I'm not making any such assumption, so your desperate evasion won't work. You might want to reread the hypothesis we're testing. Isn't it my hypothesis we're testing?   Quote     Quote You must show me that the evidence supports this assumed buildup of random mutations first, then we can move on from there. Nope. That's not how science works. We use hypotheses to make predictions, and then we look at the evidence to see whether it is consistent or inconsistent. Only pseudoscientists who have zero confidence in their hypotheses make petulant demands like yours. What demands?  My hypothesis predicts that there is no buildup of random mutations within the genome - even in non-coding sites.  Isn't that what we're testing? -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 13 2007,23:32    Speaking of predictions, I have another one for you: It's my prediction that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,00:01    Quote (Daniel Smith @ Oct. 13 2007,23:32) My hypothesis does not predict a flat line - except within a lineage.  By "lineage" I mean either the same species or very closely related species.  As an example I would think something along the lines of the African vs. Asian elephant.  This is why I said that the test needs to be done within the lineage to test my hypothesis. I already gave you a URL for such a pair--rat vs. mouse. You, predictably, completely ignored the data.     Quote But orthologous regions are regions that are thought to be homologous due to speciation - which is assumed to have occurred by an accumulation of mutations - isn't that correct?     Not even close. All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that?       Quote Isn't it my hypothesis we're testing?     We're testing both at once.       Quote What demands?       Quote You must show me that the evidence supports this assumed buildup of random mutations first, then we can move on from there. That's a petulant demand.       Quote My hypothesis predicts that there is no buildup of random mutations within the genome - even in non-coding sites.  Isn't that what we're testing? Not quite. Your hypothesis predicts that identity will be no different in coding vs. noncoding sites. Predictions are made about observable data, but we both know that you're desperate to avoid that. You really oughta figure out that "random" only refers to fitness before going on these rants.   Quote Speaking of predictions, I have another one for you: It's my prediction that random mutations are only neutral or deleterious - never advantageous. That's not a prediction, it's a hypothesis. Come on, man, this isn't that difficult. Predictions are made ABOUT DIRECTLY OBSERVABLE THINGS. Let's see if you can grasp this at the second-grade level: 1) The hypothesis that my dog understands the meaning of the word "sit" predicts that that my dog WON'T sit when I say "fit" or "tit" or "sib" or "hit" in the same tone of voice and with the same body language. 2) The hypothesis that my dog does not understand the meaning of the word "sit" predicts that that my dog WILL sit when I say "fit" or "tit" or "sib" or "hit" in the same tone of voice and with the same body language. Do you get it yet? The prediction is about what you directly observe--whether the dog sits or not.   Quote All advantageous mutations are non-random and are therefore experimentally repeatable. "Non-random"=/="experimentally repeatable," Daniel. If one does sufficient trials, the random becomes not only repeatable, but predicted. Maybe you should read a primer on the Poisson distribution.   Quote "Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72." That's meaningless without numbers, but that's probably what you were aiming for.

Richard Simons Posts: 425 Joined: Oct. 2006 (Permalink) Posted: Oct. 14 2007,00:10    Quote (daniel Smith @ Oct. 13 2007,23:32) By "lineage" I mean either the same species or very closely related species.  As an example I would think something along the lines of the African vs. Asian elephant. I could be wrong, but I thought that African and Asian elephants were considered to be less closely related than humans and chimps. Is this close enough for your purposes, Daniel? -------------- All sweeping statements are wrong.

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 14 2007,10:16    Quote (Wesley R. Elsberry @ Oct. 13 2007,16:36) Quote I see no "Edit" button with my browser (Mozilla Firefox). You should see an edit button on your own posts, but not other people's posts. With moderator privileges, the edit button is on every comment. I have no Edit button on my posts.  Not with Mozilla, not with IE. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 14 2007,10:20    [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better? -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 14 2007,10:37    Quote (JAM @ Oct. 14 2007,00:01) I already gave you a URL for such a pair--rat vs. mouse. You, predictably, completely ignored the data. I went there, but I'm not sure what I'm looking at.  What I want to see is the rat and mouse genome side by side, sequence by sequence.  That program appears to pick pieces out of the genome and line them up independently of their position in the chromosome.  Basically, I want to start at chromosome 1, bp 1, and see the rat and mouse side by side.  Is that possible? Quote       Quote But orthologous regions are regions that are thought to be homologous due to speciation - which is assumed to have occurred by an accumulation of mutations - isn't that correct?     Not even close. All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that? Designed descent. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,10:53    Quote (Daniel Smith @ Oct. 14 2007,10:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better? Better, but you still need numbers. Specifically, "rapidly" is not meaningful, because mutation rates are calculated per individual per generation. What does your hypothesis predict if a different bacterial species is selected on nylon? 1) Will multiple selections give the same result, and/or 2) Will the enzymes that evolved be the orthologs of the ones that evolved in Achromobacter? P.S. Did you check out the mouse vs. rat sequences yet?

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,11:25    Quote (Daniel Smith @ Oct. 14 2007,10:37)   Quote (JAM @ Oct. 14 2007,00:01) I already gave you a URL for such a pair--rat vs. mouse. You, predictably, completely ignored the data. I went there, but I'm not sure what I'm looking at. I told you that you were looking at mouse vs. rat in line 3, but you ignored me.   Quote What I want to see is the rat and mouse genome side by side, sequence by sequence. That's exactly what I showed you in line 3.   Quote That program appears to pick pieces out of the genome and line them up independently of their position in the chromosome. Utterly, totally false. As I plainly explained to you, this lines up orthologous regions only. If you're going to call me a liar, Daniel, at least have the integrity to do so plainly. Quote Basically, I want to start at chromosome 1, bp 1, and see the rat and mouse side by side.  Is that possible? Absolutely, as long as you're not resistant to basic education.   Quote Quote   Quote But orthologous regions are regions that are thought to be homologous due to speciation - which is assumed to have occurred by an accumulation of mutations - isn't that correct?     Not even close. All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that? Designed descent. How do you explain the breakpoints between syntenic regions in your design hypothesis, then? How do you explain the extensive synteny that crosses what you idiosyncratically define as "lineages"?

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 14 2007,14:26    Quote (Wesley R. Elsberry @ Oct. 08 2007,07:49)   Quote My prediction is that the coding and non-coding sequences (basically all sequences) will show an equal amount of evolutionary constraint. So, why does the term "linkage disequilibrium" seem to get used by geneticists? Wouldn't your prediction mean that we should see the same degree of linkage disequilibrium everywhere we look? If not, what consequences do you think your "prediction" actually has? First, here's a definition of linkage disequilibrium that I can understand:   Quote The occurrence of some genes together, more often than would be expected. Thus, in the HLA system of histocompatibility antigens, HLA A1 is commonly associated with B8 and DR3 and A2 with B7 and DR2, presumably because the combination confers some selective advantage. link Do you agree with this definition? Second, if so, I'm not sure how this applies to my hypothesis.  Why would you think that evolutioary constraint of non-coding sites would lead to "the same degree of linkage disequilibrium everywhere we look"? I guess I'm not understanding the connection. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 14 2007,14:34    First, I'm trimming the accusations that I somehow called you a liar because I don't fully understand how VISTA works.     Quote (JAM @ Oct. 14 2007,11:25)   Quote   Quote All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that? Designed descent. How do you explain the breakpoints between syntenic regions in your design hypothesis, then? How do you explain the extensive synteny that crosses what you idiosyncratically define as "lineages"? The designed descent hypothesis accepts that some genetic regions are passed on intact - while others are changed during the saltational phase of evolution.  I'm not sure how your objection applies. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,14:48    Quote (Daniel Smith @ Oct. 14 2007,14:26)   Quote (Wesley R. Elsberry @ Oct. 08 2007,07:49)       Quote My prediction is that the coding and non-coding sequences (basically all sequences) will show an equal amount of evolutionary constraint. So, why does the term "linkage disequilibrium" seem to get used by geneticists? Wouldn't your prediction mean that we should see the same degree of linkage disequilibrium everywhere we look? If not, what consequences do you think your "prediction" actually has? First, here's a definition of linkage disequilibrium that I can understand:       Quote The occurrence of some genes together, more often than would be expected. Thus, in the HLA system of histocompatibility antigens, HLA A1 is commonly associated with B8 and DR3 and A2 with B7 and DR2, presumably because the combination confers some selective advantage. link Do you agree with this definition? "Genes" should be "alleles." Do you understand the difference? It's essential for understanding the concept.   Quote Second, if so, I'm not sure how this applies to my hypothesis.  Why would you think that evolutioary constraint of non-coding sites would lead to "the same degree of linkage disequilibrium everywhere we look"? I'd rephrase what Wesley said and point out that your hypothesis predicts that linkage disequilibrium shouldn't be found at all.   Quote I guess I'm not understanding the connection. It's interesting that you implicitly claim to understand biology sufficiently to claim that you understand it better than we biologists do, but every time someone points to major problems in reconciling it with the data, you become incredibly modest about your intellect. Do you not see an inconsistency there?

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,14:59    Quote (Daniel Smith @ Oct. 14 2007,14:34) First, I'm trimming the accusations that I somehow called you a liar because I don't fully understand how VISTA works.   You were implying that I wasn't honest despite the fact that I explicitly explained to you that line 3 represented mouse vs. rat, and you complained that "What I want to see is the rat and mouse genome side by side, sequence by sequence." That was precisely what I was showing you. Now, I'm asking if you want to see it.       Quote (JAM @ Oct. 14 2007,11:25)       Quote       Quote All orthologs are homologs, but not all homologs are orthologs. Orthologs are not merely homologous, but have the same function. Operationally, we're only really sure about these when we have complete genome sequences or when we rescue a mouse mutant with its human ortholog as a transgene. There are orthologous stretches along huge segments of chromosomes, in which gene order is preserved. This is called synteny. How do you explain that? Designed descent. How do you explain the breakpoints between syntenic regions in your design hypothesis, then? How do you explain the extensive synteny that crosses what you idiosyncratically define as "lineages"?   Quote The designed descent hypothesis accepts that some genetic regions are passed on intact - Hypotheses don't "accept" things, people do. Hypotheses predict. What percentage of the genome do you mean by "some," Daniel?   Quote ... while others are changed during the saltational phase of evolution.  I'm not sure how your objection applies. I didn't offer an objection. I asked you questions that you are evading. Let's try again. Synteny refers to intact gene orders, not intact sequences. See if you can answer two questions straight up: 1) When considering man/mouse synteny, what proportion of the genome will retain gene orders? 2) Again, with man vs. mouse (but not synteny), each has ~30,000 genes. According to your hypothesis, how many human genes won't have a mouse ortholog and vice versa? Honest answers will be in numerical form.

jeannot Posts: 1201 Joined: Jan. 2006 (Permalink) Posted: Oct. 14 2007,15:40    Quote (JAM @ Oct. 14 2007,14:48) I'd rephrase what Wesley said and point out that your hypothesis predicts that linkage disequilibrium shouldn't be found at all. I don't see how Daniel's hypothesis contradicts linkage disequilibrium. He's not implying that a locus undergoes the same selective pressure whatever its genomic background, he's implying that non-coding regions and genes are subject to the same level of selection, on average. Of course, this relies on other evolutionary mechanisms (namely genetic epistasis) that Daniel may reject.

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 14 2007,15:43    Quote (jeannot @ Oct. 14 2007,15:40) Quote (JAM @ Oct. 14 2007,14:48) I'd rephrase what Wesley said and point out that your hypothesis predicts that linkage disequilibrium shouldn't be found at all. I don't see how Daniel's hypothesis contradicts linkage disequilibrium. He's not implying that a locus undergoes the same selective pressure whatever its genomic background, he's implying that non-coding regions and genes are subject to the same level of selection, on average. Is that right, Daniel? That all depends on whether "on average" is a part of it, I'd say.

jeannot Posts: 1201 Joined: Jan. 2006 (Permalink) Posted: Oct. 14 2007,15:51    Quote (JAM @ Oct. 14 2007,15:43)   Quote (jeannot @ Oct. 14 2007,15:40)   Quote (JAM @ Oct. 14 2007,14:48) I'd rephrase what Wesley said and point out that your hypothesis predicts that linkage disequilibrium shouldn't be found at all. I don't see how Daniel's hypothesis contradicts linkage disequilibrium. He's not implying that a locus undergoes the same selective pressure whatever its genomic background, he's implying that non-coding regions and genes are subject to the same level of selection, on average. Is that right, Daniel? That all depends on whether "on average" is a part of it, I'd say. Well, it's clear that Daniel is not familiar with recombination and genetic epistasis. He just thinks that a designer would not inject big chunks of useless DNA in our streamlined genome. If that's his only contention with the ToE, linkage disequilibrium remains. I'd like to hear his explanation about the Alu sequences, though. EDIT: I should add that genetic drift leads to linkage disequilibrium if there is population structure. Apparently, Daniel accept that synonymous sites are neutral so I conclude that his hypothesis doesn't say much about drift.

David Holland Posts: 17 Joined: Oct. 2007 (Permalink) Posted: Oct. 15 2007,15:51    Quote (Daniel Smith @ Oct. 14 2007,10:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better? [QUOTE] I want to go back to this one for a minute. Suppose I set up a vat with a bazillion Acromobacter guttatus and nylon as the primary source of carbon. If one of the bacteria developes the ability to digest nylon has your hypothesis been supported? Without numbers I can't tell.

Henry J Posts: 5786 Joined: Mar. 2005 (Permalink) Posted: Oct. 15 2007,22:23    Quote Suppose I set up a vat with a bazillion Acromobacter guttatus and nylon as the primary source of carbon. I dunno - there might be too many things that could hose that experiment, so I wouldn't put too much stocking into it. Henry

Steverino Posts: 411 Joined: Oct. 2005 (Permalink) Posted: Oct. 16 2007,06:36    "The designed descent hypothesis accepts that some genetic regions are passed on intact - while others are changed during the saltational phase of evolution.  I'm not sure how your objection applies."  - Denial Smith AAHHHH>....Creation thru unidentifiable-all powerful widget. -------------- - Born right the first time. - Asking questions is NOT the same as providing answers. - It's all fun and games until the flying monkeys show up!

JonF Posts: 634 Joined: Feb. 2005 (Permalink) Posted: Oct. 16 2007,07:19    Quote (Daniel Smith @ Oct. 14 2007,11:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better? Better, but still not good enough.  Yuu need to quantify "too rapidly". Numbers.

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 16 2007,14:00    [quote=David Holland,Oct. 15 2007,15:51]   Quote (Daniel Smith @ Oct. 14 2007,10:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better? Quote I want to go back to this one for a minute. Suppose I set up a vat with a bazillion Acromobacter guttatus and nylon as the primary source of carbon. If one of the bacteria developes the ability to digest nylon has your hypothesis been supported? Without numbers I can't tell. Only if it develops the same exact frame shift and only if it happens consistenty faster than random mutation rates can account for. BTW, I don't have any idea what those rates are, but I'm sure whoever was doing the test would get that info first. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

swbarnes2 Posts: 78 Joined: Mar. 2006 (Permalink) Posted: Oct. 16 2007,14:34    Quote Only if it develops the same exact frame shift Okay, so let's get this straight. Do you agree that the ability to resist antibiotics is "beneficial"? If so, you then predict that if 50 labs all over the country screen put every post-doc and lab tech they had to work screening plates for 3 months to find resistant mutants, they will ALL find the exact same mutation? What if I'm screening for a mutation that cripples a certain pathway, and when I find a colony with the mutation I want, I will keep it and cultivate it for the next 20 years, and all the other ones just get incinerated. Doesn't that make that mutation beneficial?  You certainly can't claim that its bearers fare worse in their environment than the wild-type kind.

JAM Posts: 517 Joined: July 2007 (Permalink) Posted: Oct. 16 2007,15:07    Quote (Daniel Smith @ Oct. 16 2007,14:00) [quote=David Holland,Oct. 15 2007,15:51]   Quote (Daniel Smith @ Oct. 14 2007,10:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better?   Quote I want to go back to this one for a minute. Suppose I set up a vat with a bazillion Acromobacter guttatus and nylon as the primary source of carbon. If one of the bacteria developes the ability to digest nylon has your hypothesis been supported? Without numbers I can't tell. Only if it develops the same exact frame shift and only if it happens consistenty faster than random mutation rates can account for. BTW, I don't have any idea what those rates are, but I'm sure whoever was doing the test would get that info first. What does your hypothesis predict if a different bacterial species is selected on nylon? 1) Will multiple selections give the same result, and/or 2) Will the enzymes that evolved be the orthologs of the ones that evolved in Achromobacter? P.S. Did you check out the mouse vs. rat sequences yet?

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 16 2007,18:44    [quote=JAM,Oct. 16 2007,15:07]   Quote (Daniel Smith @ Oct. 16 2007,14:00)     Quote (David Holland @ Oct. 15 2007,15:51)         Quote (Daniel Smith @ Oct. 14 2007,10:20) [EDIT] Speaking of predictions, I have another one for you: It's my hypothesis that random mutations are only neutral or deleterious - never advantageous.  All advantageous mutations are non-random and are therefore experimentally repeatable and will occurr too rapidly to be random. Therefore, I predict that anytime Acromobacter guttatus Sp. K172 is subjected to an environment where it must consume nylon to survive, the same frame shift will occur, resulting in Flavobacterium Sp. KI72. Better?       Quote I want to go back to this one for a minute. Suppose I set up a vat with a bazillion Acromobacter guttatus and nylon as the primary source of carbon. If one of the bacteria developes the ability to digest nylon has your hypothesis been supported? Without numbers I can't tell. Only if it develops the same exact frame shift and only if it happens consistenty faster than random mutation rates can account for. BTW, I don't have any idea what those rates are, but I'm sure whoever was doing the test would get that info first. What does your hypothesis predict if a different bacterial species is selected on nylon? I've already made my prediction, why are asking me to make another one?     Quote 1) Will multiple selections give the same result, and/or 2) Will the enzymes that evolved be the orthologs of the ones that evolved in Achromobacter? My prediction was that exactly the same frame shift will occur - so I'm guessing it will be #1.       Quote P.S. Did you check out the mouse vs. rat sequences yet? I've been there several times.  Let me give you a blow by blow of my most recent visit: I want to see the mouse and rat genomes side by side so I go to VISTA and select the Mouse Feb. 2006 genome as a base genome, then I figure the best place to start is at the beginning, so I select ch1:1-1000000 and click GO, I get an error saying "No such contig. or chromosome".  This is a bit confusing.  How can the mouse genome not have a chromosome 1?  So then I select ch2:1-1000000 and get the same error. Ch3 and 4 give the same results. So then I decided to try the Rat June 2003 and go with the default chr10:10000001-10100000, which then gives me some results.  I click on Browse alignment so I can see the coding (the Cs, As, Ts, and Gs).  I zoom in on a spot and when I put my mouse over the Rat code, it gives the number 10034062, when I cursor over the Mouse genome in the same spot, it gives the number 5312532.  I'm assuming these are the numbers for the position of that site within the chromosome.  So, (if that's the case) it's not showing me the Rat and Mouse genomes, side by side - starting at position 10000001 and ending at position 10100000.  If it was, they'd both give the number 10034062 - wouldn't they? So, like I said, I'm not sure what I'm looking at and I'm not sure the correct way to use the site, but it doesn't appear to be giving me what I was looking for.  So, if you have something you want me to see, you'll have to specifically tell me what it is I'm looking at and how it reflects on my hypothesis. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 16 2007,18:53    Quote (mitschlag @ Oct. 13 2007,18:22)   Quote (Daniel Smith @ Oct. 13 2007,13:53)       Quote (mitschlag @ Oct. 10 2007,12:47)         Quote (Daniel Smith @ Oct. 10 2007,02:30) The results that would falsify my hypothesis would be if the coding sequences showed evolutionary constraint while the non-coding sequences didn't. There's a fair amount of evidence showing that (contrary to expectation) non-coding sequences have fewer base changes than coding sequences, see, for example: http://www.biomedcentral.com/1471-2148/7/66           Quote The primary result is that the mean rate of intergenic nucleotide substitution is two-thirds that of the synonymous coding data, with an absolute rate estimated to be 1.05 × 10-8 substitutions per site per year. This result holds with alternative nucleotide models (see Methods), and thus does not appear to be solely an issue of estimation procedures. Slower rates in non-coding regions relative to synonymous sites are becoming a surprisingly frequent observation. For example, a recent study of Drosophila demonstrated that non-coding DNA evolves considerably slower than synonymous sites in terms of both divergence between species and polymorphism within species [16]. By comparing studies, one can also make the case that pseudogenes [32,33] and introns [34,35] evolve more slowly than synonymous sites in apes and other mammals [13,36-38]. Studies of mammalian intergenic regions have also found slower rates than synonymous sites [35,39,40]. Although most of these studies encompass only a handful of genes, an overall picture of relatively slow non-coding rates is emerging. What do you make of that? If this is true, then it would be a confirmation of my hypothesis with better than expected results. It's true, all right, but it doesn't confirm your hypothesis. To learn why, read the cited paper.  Hint: TE=transposable element. (Sorry that I won't be able to participate in this discussion for the next two weeks due to travel in arcane regions.  In the meantime, I want to commend DS for  his courteous and patient responses to the many challenges that have been addressed to him.) I read the cited paper.  It was very interesting - a bit over my head - but interesting nonetheless. Your suggestion to read up on transposable elements was very fruitful as well as now these have piqued my interest.  I, of course, don't believe these to be randomly generated or to be degenerate copies of working genes.  I think they are more likely functional switches for some as yet undefined purpose.  I'm going to read more about them. Oh and thanks for the commendation.  I appreciate a good civil discussion.  Unfortunately, when things get hostile, I have a tendency to get my guard up and push back a little harder than I have the right to.  Thanks for putting up with that as well. -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

Daniel Smith Posts: 970 Joined: Sep. 2007 (Permalink) Posted: Oct. 16 2007,18:55    Quote (swbarnes2 @ Oct. 16 2007,14:34) Quote Only if it develops the same exact frame shift Okay, so let's get this straight. Do you agree that the ability to resist antibiotics is "beneficial"? If so, you then predict that if 50 labs all over the country screen put every post-doc and lab tech they had to work screening plates for 3 months to find resistant mutants, they will ALL find the exact same mutation? What if I'm screening for a mutation that cripples a certain pathway, and when I find a colony with the mutation I want, I will keep it and cultivate it for the next 20 years, and all the other ones just get incinerated. Doesn't that make that mutation beneficial?  You certainly can't claim that its bearers fare worse in their environment than the wild-type kind. I made a specific prediction.  Why do you want me to modify it to fit your scenario? -------------- "If we all worked on the assumption that what is accepted as true is really true, there would be little hope of advance."  Orville Wright "The presence or absence of a creative super-intelligence is unequivocally a scientific question."  Richard Dawkins

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