tag:blogger.com,1999:blog-37148773.post1140816617712180117..comments2024-03-27T14:50:47.345-04:00Comments on <center>Sandwalk</center>: Intelligent design needs to clean up its act if it expects to be taken seriouslyLarry Moranhttp://www.blogger.com/profile/05756598746605455848noreply@blogger.comBlogger405125tag:blogger.com,1999:blog-37148773.post-39584893839775386572015-11-05T04:34:28.629-05:002015-11-05T04:34:28.629-05:00Max, read and try to understand these two posts:
...Max, read and try to understand these two posts:<br /><br /><a href="http://sandwalk.blogspot.nl/2015/11/molecular-evidence-supports-evolution.html" rel="nofollow">http://sandwalk.blogspot.nl/2015/11/molecular-evidence-supports-evolution.html</a><br /><br />and this one:<br /><a href="http://sandwalk.blogspot.nl/2015/11/the-birth-and-death-of-salmon-genes.html" rel="nofollow">http://sandwalk.blogspot.nl/2015/11/the-birth-and-death-of-salmon-genes.html</a><br /><br />Now, with your knowledge of evolution, do explain why the conclusions in these posts are wrong.<br />After you've finished with the first part, now comes the hard part, explain how design explains the gene duplication event better. Questions I'd like to see answered are, but not limited to:<br />- why wasn't the duplication already designed in?<br />- why do some fish in this line have the duplication, while others lack it? <br />- looking at the sequence data, explain how this duplication event happened because one of the premisses of ID is that evolution can't add information. The sequence data tells us, there was a common ancestor before the duplication happened, the logical conclusion is that the design was made before the duplication event. <br />- Looking at the first post, the data tells us many (precursor) species where already present before the cambrium explosion kicked off. Some/many ID proponents say the cambrium was the starting point for the designer. The data shows something different. Explain please.<br />- Could you explain the error the authors of the paper made in the humanoid line? It seems the sequence data shows a common ancestor with monkeys. Can you explain why the sequence data is wrong?<br /><br />I'm really looking forward to your answers. <br />Edhttps://www.blogger.com/profile/15924368353226400878noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-8978742552553634252015-11-04T06:58:07.030-05:002015-11-04T06:58:07.030-05:00Yes, Bill Cole. Or, if not a link, at least some ...Yes, Bill Cole. Or, if not a link, at least some clearer directions. I can't even tell what website you're talking about.<br /><br />I also want to reiterate my main point, because it is really very simple. If you still need to think about it, it must be because I did not explain it clearly.<br /><br />You keep bringing up the "sequence space" and saying that, for the degree of difference between proteins found in chimps and humans, it must be necessary for the genes coding for these proteins to have "worked thru" this sequence space. But that is simply not the case. If two proteins are, say, 95% similar, then it is only necessary that they undergo enough random mutations to account for this 5% difference. Empirical evidence demonstrates that the observed mutation rate can easily account for this.<br /><br />Back to the earlier analogy: If you blindfold someone and place him at a house only three doors away from yours, there is a very high probability, that, given enough trials he will eventually make it to your door, just by chance.<br /><br />However, if we blindfold him and place him on an asteroid in the Andromeda Galaxy, it would be, for all practical purposes, impossible for him to get to your door. <br /><br />Your problem is you are failing to distinguish between these two scenarios. If those two 95% similar proteins arose completely from scratch in unrelated organisms that shared no common ancestor, and that similarity was arrived at by randomly traversing the sequence space, then you're correct. That odds against that are probably insurmountable.<br /><br />But that's not what happened. Those two proteins arose from an ancestor that was only about 5% (or less) different from either of them.<br /><br />Your argument is like saying your friend could not possibly have made it to your door from another house three doors down, because he would have had to travel the entire expanse of space between your house and the Andromeda Galaxy. I hope you now realize why that is nonsense. Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-74847335677124687562015-11-04T03:00:57.671-05:002015-11-04T03:00:57.671-05:00Can you post a link please Bill? Can you post a link please Bill? Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-89817345215915830182015-11-03T22:36:51.732-05:002015-11-03T22:36:51.732-05:00Hi Lutesuite
All the above points are relevant res...Hi Lutesuite<br />All the above points are relevant respectfully well stated. Have some business issues that are pressing right now. Want to spend time thinking about it so I can communicate as well as you have. The discussion is on junk DNA (Larry) and ape to man transition (Nick). If you look for Nicks name at the front of the webpage you can click on it and read the discussion. Your thoughtful questions are much appreciated.Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-37362240619563257952015-11-03T11:35:37.002-05:002015-11-03T11:35:37.002-05:00You guys should read through Larry and Nicks discu...<i>You guys should read through Larry and Nicks discussion on common decent. This subject is debated there.</i><br /><br />Which discussion is that?<br />Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-79922371798987339172015-11-03T11:27:12.891-05:002015-11-03T11:27:12.891-05:00First question is a conservative estimate from the...<i>First question is a conservative estimate from the genome data comparison and estimates I have heard of. I can include back up data if you guys think it is important.</i><br /><br />Yes, I think it's important to this discussion. So please provide the source.<br /><br /><i>Novel means more than a few mutations where the protein needs to find a new function.</i><br /><br />That's still a very vague definition. Maybe you could provide an specific example of one of these proteins you have in mind.<br /><br /><i>I honestly think it is a long shot that 100 exons were deleted....</i><br /><br />Why do you think this? Could you provide the scientific evidence that shows this to be unlikely? <br /><br /><i>The blind man leaving the house in a random direction is a good analogy for finding functioning protein space. Hunts paper describes that this space is rare. His data creates a problem for the ape to man transition by random change even with his most conservative estimates.</i><br /><br />Really? Have a look at the 4th graph in his paper. What kind of "problem" do you think that represents?<br /><br />You're also on the wrong track if you think it's one blind man trying to find one functioning protein spaces. It's actually millions of blind men trying to find any one of millions of functioning spaces. That makes a big difference.<br /> <br /><br /><br />Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-68275546337241435582015-11-03T11:13:34.018-05:002015-11-03T11:13:34.018-05:00Hi Lutesuite
On what basis do you claim there are...Hi Lutesuite<br /><br />On what basis do you claim there are 60 novel human proteins? What is your definition of "novel"?<br /><br />Are you now retracting your agreement with Larry that the difference between the human and chimp versions of titin could have resulted merely from the deletion of 25 exons?<br /><br />First question is a conservative estimate from the genome data comparison and estimates I have heard of. I can include back up data if you guys think it is important. Novel means more than a few mutations where the protein needs to find a new function.<br /><br />Larry's idea is certainly valid to test. I honestly think it is a long shot that 100 exons were deleted from chimps but there is no data to rule it out at this point.<br />I would really like to explore this one.<br /><br />The blind man leaving the house in a random direction is a good analogy for finding functioning protein space. Hunts paper describes that this space is rare. His data creates a problem for the ape to man transition by random change even with his most conservative estimates.<br /><br />You guys should read through Larry and Nicks discussion on common decent. This subject is debated there.<br /><br />I will try to get to more when I get home tonight.Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-8838156486357890492015-11-03T09:02:53.039-05:002015-11-03T09:02:53.039-05:00The weird thing, Dazz, is that Bill Cole keeps cit...The weird thing, Dazz, is that Bill Cole keeps citing this article by Art Hunt as evidence in support of his position:<br /><br />https://aghunt.wordpress.com/2008/12/26/axe-2004-and-the-evolution-of-enzyme-function/<br /><br />However, that article is actually arguing <i>against</i> Bill Cole's position, and provides evidence to reject it. Bill Cole's argument is that the sequence space resembles Figure 3 in that article: Extremely narrow and widely spaces islands of functional sequences among a vast desert of non-functional sequences. But Hunt argues that Figure 4 is the more accurate depiction. It makes me wonder if Bill Cole even understands his own argument.<br />Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-30242049219265533112015-11-03T00:27:10.020-05:002015-11-03T00:27:10.020-05:00let me know if 50 million mutations can get you 60...<i>let me know if 50 million mutations can get you 60 novel human proteins? </i><br /><br />Do you understand <a href="http://sandwalk.blogspot.ca/2012/01/whats-difference-between-human-and.html" rel="nofollow">the math involved in genetic drift?</a> It doesn't even consider natural selection, just neutral fixations:<br /><br /><i>How many mutations would we expect in the human lineage since it diverged from a common ancestor with chimpanzees if all of the fixed alleles were neutral? The two species diverged about 5 million years ago. The average generation time in the human lineage is about ten years, so that means 500,000 generations. If the rate of mutation is about 100 new mutations per generation, then we would expect to see about 50 million new mutations in the human lineage. The actual number is about 22.5 million (half of 45 million). We're certainly in the right ballpark.<br /><br />The actual mutation rate may be lower than we calculate.<br /><br />We're certainly safe in concluding that the number of differences between humans and chimps is consistent with Neutral Theory and we should accept this as the null hypothesis.</i><br /><br />our geno is about 3000Mbp long. 1% difference is about 30M fixations. <br />If 10% of the geno codes for proteins, then would be 3M fixations in protein coding DNA. I guess those would be subject to higher selective pressure, but still<br /><br />So the answer to me is clearly yes, 50M mutations can in fact get you 60 novel proteins... by genetic drift alone. <br /><br />You keep assuming the sequence space is a vast desert, in the face of the evidence. Just look at the Titin, look at all the different versions of it in all the species, I just run BLAST against the Japanese rice fish's Titin and the match was 65% with human Titin. That's quite a difference and it's still doing fine. It clearly suggests that there are many, many viable versions of a protein and the known mechanisms can explain the diversity just fineDazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-23644744385325299732015-11-02T21:38:07.491-05:002015-11-02T21:38:07.491-05:00Once he has arrived yes it is 100% but when he lea...<i>Once he has arrived yes it is 100% but when he leaves he has to find a destination where he can become a functioning protein</i><br /><br />No, he doesn't. He just has to move to another similar protein with roughly the same function. Nearly neutral theory demonstrates that these abound.<br /><br />The case you have been discussing is titin. How many mutations can occur in this with it remaining functional? Remember, there are 11 structurally distinct isoforms in humans alone.<br /><br /><i>let me know if 50 million mutations can get you 60 novel human proteins</i><br /><br />On what basis do you claim there are 60 novel human proteins? What is your definition of "novel"?<br /><br />Are you now retracting you agreement with Larry that the difference between the human and chimp versions of titin could have resulted merely from the deletion of 25 exons? Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-26776107408676732852015-11-02T21:03:04.645-05:002015-11-02T21:03:04.645-05:00Again, that is the wrong question, if you wish to ...Again, that is the wrong question, if you wish to create an analogy to the process of evolution. The correct question is "Your friend starts in a random direction blindfolded. After a period of time he arrives at a random destination. Once he has arrived at that destination, what are the odds that he has arrived at that destination?" The answer, in case you can't figure it out yourself, is 100%.<br />Once he has arrived yes it is 100% but when he leaves he has to find a destination where he can become a functioning protein and as we move down the evolutionary path those options get smaller. We are not dealing exclusively with natural selection and large bacterial populations so re read the above section you sent me and let me know if 50 million mutations can get you 60 novel human proteins? The best case for 1 is 10^10 and that is for 100 amino acid sequences which is 20% the size of an average human protein.Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-86774864805103033942015-11-02T20:41:03.418-05:002015-11-02T20:41:03.418-05:00In this case the person knows the direction to the...<i>In this case the person knows the direction to the house. If mutations occur and evolution does not know where its going how does it find the next working protein? It may have a few mutations and have no effect but how does it find a new function? Or a modified function? It does not know where its going and its traveling in huge sequential space.</i><br /><br />That is a weakness in my analogy, true. The friend is actually trying to get to your house.<br /><br />You don't seem to realize the assumption you are making, however: The protein that has been modified by mutation is not "looking" for a new function. It just, in a small minority of cases, might by luck happen to find a new function.<br /><br />You are assuming that evolution is seeking a particular objective. If you assume that, then of course it will have to be "directed" in some way if it is to find that objective. But first you have to demonstrate mutations are, in fact, occurring with the goal of achieving an objective such as a new or improved function. You have yet to do so. Neither has anyone else. So, again, you are committing the error you accuse others of doing, and assuming things to be true that have not been demonstrated by the scientific method. <br /><br /><i>Your friend leaves your house and starts in a random direction blind folded. Whats the chance he runs into his house? How about the chance he runs into an specific spec of sand on the Andromeda Galaxy traveling from your house blindfolded in a random direction. </i><br /><br />Again, that is the wrong question, if you wish to create an analogy to the process of evolution. The correct question is "Your friend starts in a random direction blindfolded. After a period of time he arrives at a random destination. Once he has arrived at that destination, what are the odds that he has arrived at that destination?" The answer, in case you can't figure it out yourself, is 100%.<br /><br />You keep alluding to Art Hunt. Is that the same Art Hunt who wrote this:<br /><br /><i>10^-10 -> 10^-63 (or thereabout): this is the range of estimates of the density of functional sequences in sequence space that can be found in the scientific literature.... To give the reader a sense of the higher end (10^-10) of this range, it helps to keep in mind that 1000 liters of a typical pond will likely contain some 10^12 bacterial cells of various sorts. If each cell gives rise to just one new protein-coding region or variant (by any of a number of processes) in the course of several thousands of generations, then the probability of occurrence of a function that occurs once in every 10^10 random sequences is going to be pretty nearly 1. In other words, 1 in 10^10 is a pretty large number when it comes to “probabilities” in the biosphere.</i><br /><br /><br />If so, it sounds to me like he's not really saying what you think he's saying. Ooops!Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-82276452478408433312015-11-02T18:58:13.196-05:002015-11-02T18:58:13.196-05:00Hi Lutesuite
That's the same as, if your frie...Hi Lutesuite<br /><br />That's the same as, if your friend asks why you think he must have traveled thru the Andromeda Galaxy to get to his house, you just keep regaling him with accounts of how vast and distant the Andromeda Galaxy is<br /><br />In this case the person knows the direction to the house. If mutations occur and evolution does not know where its going how does it find the next working protein? It may have a few mutations and have no effect but how does it find a new function? Or a modified function? It does not know where its going and its traveling in huge sequential space. See Art Hunts paper. Your friend leaves your house and starts in a random direction blind folded. Whats the chance he runs into his house? How about the chance he runs into an specific spec of sand on the Andromeda Galaxy traveling from your house blindfolded in a random direction. Again, mathematical spaces of proteins are larger then the number of atoms in the known universe ....how do you get from protein A to protein B traveling through this enormous space with random change? You say small stops along the way...according to Hunts paper the smallest stops are 10^10 between each other and average 10^32. Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-61100554425700886412015-11-02T18:18:47.940-05:002015-11-02T18:18:47.940-05:00You're still missing the main point, Bill Cole...You're still missing the main point, Bill Cole. There is no need to provide a testable hypothesis that is an alternative to having to "work through the sequential space and change proteins" because it is simply obvious to anyone who understands the relevant issues that is not necessary to "work thru the sequential space." Your proposal does not need to be refuted because it is patent nonsense.<br /><br />Suppose a friend arrived at your house and, when you asked him how he got there, he said he just walked from the next block. And suppose you insist you do not believe him, and that he must first prove that he did not travel thru the Andromeda Galaxy on the way to your house. That's the equivalent of the argument you keep making about the "sequential space."<br /><br /><i>Larry's idea is another way that a protein can change without working through sequential space . These are ideas you guys have not been talking about before.</i><br /><br />That is false. Larry's idea is no more than the same one Dazz and I have been repeating to you: That the two proteins simply arose from a common ancestor thru random mutations. That you failed to understand what we were writing is not our fault.<br /><br />You have yet to explain why you persist in believing that any minor modification to an existing protein requires "working thru the sequential space" of all possible combinations of amino acids. All you do is keep repeating how vast this number of combinations is. So what? That's the same as, if your friend asks why you think he must have traveled thru the Andromeda Galaxy to get to his house, you just keep regaling him with accounts of how vast and distant the Andromeda Galaxy is. Do you think that answers his question? Do you think such an argument is even worth taking seriously? Or should your friend think you're either daft or just pulling his leg? That's how you're coming across here.Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-63573877641567615592015-11-02T16:32:59.447-05:002015-11-02T16:32:59.447-05:00Hi Dazz lutesuite...I do not have a testable hypot...Hi Dazz lutesuite...I do not have a testable hypothesis for design. Yes, alternative splicing is a way to not work through the sequential space and change proteins. Larry's idea is another way that a protein can change without working through sequential space . These are ideas you guys have not been talking about before. Why not? Is this blog just about debating creationists?<br />Lutesuite...I need to think about your question about final cause more. I agree it needs to be defined. <br /><br />If you thought this was my hypothesis I miss spoke sorry.<br /><br />Your "hypothesis" was that it is impossible to arrive at the differences between the titin proteins of humans and chimps without "working thru the sequence space." Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-12731329579342345202015-11-02T15:59:29.811-05:002015-11-02T15:59:29.811-05:00Come to think of it, what exactly is "final c...Come to think of it, what exactly is "final cause", anyway, Bill Cole? Are you sure it's not just another term you're throwing around without it meaning anything, like you were with the term "directed"?<br /><br />Is there a reason you didn't answer my question? Here it is again: <br /><br />Suppose one were to also say "Getting a testable final cause like gravity vs. invisible fairies etc. as the cause of the curvature of space/time is very difficult." That is just as sensible a statement as what you wrote above, yes? <br /><br /><i>When you successfully test Larry's hypothesis then it will be disposed of.</i><br /><br />Your "hypothesis" was that it is impossible to arrive at the differences between the titin proteins of humans and chimps without "working thru the sequence space." Larry provided an example of how this difference could arise without "working thru the sequence space," and you admitted this was "certainly possible". The fact that you nonetheless refuse to admit that this falsifies your hypothesis indicates you are not actually willing to "go wherever this discussion leads us" and are not discussing in good faith. That you're just another creationist liar, to put it plainly.<br />Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-24726151097150714762015-11-02T15:53:01.713-05:002015-11-02T15:53:01.713-05:00When you successfully test Larry's hypothesis ...<i>When you successfully test Larry's hypothesis then it will be disposed of.</i><br /><br />LMFAO, talk about assuming your conclusions. And you did it again. Neutral theory has been tested. Comparing genomes shows that the difference between our genome and chimps', gorillas, etc... all differ by the expected amount by neutral fixation... across the board! <br /><br />But please, enlighten us, what testable hypothesis do you have based on "design"?. I mean a POSITIVE case for design, not one that involves ruling out naturalistic causes (by ignoring the evidence)Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-40333775852434913482015-11-02T15:44:30.455-05:002015-11-02T15:44:30.455-05:00lutesuite
I agree. Testable final causes are toug...lutesuite<br />I agree. Testable final causes are tough.<br /><br />Suppose one were to also say "Getting a testable final cause like gravity vs. invisible fairies etc. as the cause of the curvature of space/time is very difficult." That is just as sensible a statement as what you wrote above, yes?<br /><br />I really want to start do look at science between fossils/gene data and final cause. The only reason for talking about the probability data is show that final cause is tough and start talking about stuff we can test. <br /><br />BTW, whatever happened to your worries about "working thru the sequence space"? Since Larry neatly disposed of that, you no longer seem interested in talking about it. Why is that?<br /><br />When you successfully test Larry's hypothesis then it will be disposed of.<br /><br /><br />Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-90379884301452910042015-11-02T15:40:57.027-05:002015-11-02T15:40:57.027-05:00Oh, and of course...
a testable final cause like ...Oh, and of course...<br /><br /><i>a testable final cause like <b>design</b> vs natural selection neutral theory etc</i><br /><br />Design is not a (scientific) thing. It doesn't belong there with the other mechanisms. It's utterly dishonest of you to demand the amount and detail evidence in support of some mechanisms and ignore the fact that "design" has no mechanism whatsoever and makes no positive case for anything. <br /><br />Nevertheless I think we've provided all the positive evidence you demanded in support of well known mechanisms with tons of explanatory power, including the math, yet you insist in denying it all. It's not that you've argued against the evidence, you just keep hand-waiving and pretending it never happened. <br /><br />You were obviously lying when you said you were willing to go wherever this discussion led us<br /><br />Creationist dishonesty 101Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-19920861414478681302015-11-02T15:14:32.069-05:002015-11-02T15:14:32.069-05:00@Bill Cole
Hopefully you can see now that getting...@Bill Cole<br /><br /><i>Hopefully you can see now that getting a testable final cause like design vs natural selection neutral theory etc is very difficult. </i><br /><br />Suppose one were to also say "Getting a testable final cause like gravity vs. invisible fairies etc. as the cause of the curvature of space/time is very difficult." That is just as sensible a statement as what you wrote above, yes?<br /><br />BTW, whatever happened to your worries about "working thru the sequence space"? Since Larry neatly disposed of that, you no longer seem interested in talking about it. Why is that?<br /><br /><i>My point is that there are lots of Science to do between those points and fossil records and gene data. I hope you can also see that if come up with a premature answer it can stop the science because you start restricting the possible solutions in your mind.</i><br /><br />You're preaching to the choir. No one here is advocating coming up with premature answers and not testing them. No one, that is, other than the IDiots and other creationists who frequently "contribute" here. Your time would be better spent on a creationist website like Uncommon Descent, whether the only "scientific" investigation performed is that which they think can support their presumed conclusion that 'Goddidit." Faizal Alihttps://www.blogger.com/profile/00937075798809265805noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-40426197586535335242015-11-02T14:48:43.016-05:002015-11-02T14:48:43.016-05:00Hopefully you can see now that getting a testable ...<i>Hopefully you can see now that getting a testable final cause like design vs natural selection neutral theory etc is very difficult</i><br /><br />Wow, Bill, that's insanely stupid. You just keep ignoring everything we tell you, all the evidence to support that the "final cause" is well supported by evidence.<br /><br />You: <i>Where's the evidence?</i><br /><br />Us: <i>Here it is</i><br /><br />You: <i>So no evidence? Where's the evidence?</i><br /><br />Us: <i>Again, here it is!</i><br /><br />You: <i>So no evidence? Where's the evidence?...</i>Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-34115721465208212002015-11-02T14:42:54.881-05:002015-11-02T14:42:54.881-05:00OK, I found this: Regulatory Elements for TTN Gene...OK, I found this: <a href="http://www.genecards.org/cgi-bin/carddisp.pl?gene=TTN" rel="nofollow">Regulatory Elements for TTN Gene: Transcription factor binding sites by QIAGEN in the TTN gene promoter: IRF-1 HNF-1 HNF-1A STAT1 STAT1alpha STAT1beta</a><br /><br />So apparently, (some of?) the regulatory genes are in fact known.<br /><br />What if we compare those genes in humans and chimps?<br /><br /><a href="http://www.uniprot.org/uniprot/P10914.fasta" rel="nofollow">Human IRF1</a><br /><br /><b>>sp|P10914|IRF1_HUMAN Interferon regulatory factor 1 OS=Homo sapiens GN=IRF1 PE=1 SV=2<br />MPITRMRMRPWLEMQINSNQIPGLIWINKEEMIFQIPWKHAAKHGWDINKDACLFRSWAI<br />HTGRYKAGEKEPDPKTWKANFRCAMNSLPDIEEVKDQSRNKGSSAVRVYRMLPPLTKNQR<br />KERKSKSSRDAKSKAKRKSCGDSSPDTFSDGLSSSTLPDDHSSYTVPGYMQDLEVEQALT<br />PALSPCAVSSTLPDWHIPVEVVPDSTSDLYNFQVSPMPSTSEATTDEDEEGKLPEDIMKL<br />LEQSEWQPTNVDGKGYLLNEPGVQPTSVYGDFSCKEEPEIDSPGGDIGLSLQRVFTDLKN<br />MDATWLDSLLTPVRLPSIQAIPCAP</b><br /><br /><a href="http://www.uniprot.org/uniprot/H2QRG4.fasta" rel="nofollow">Chimp IRF1</a><br /><br /><b>>tr|H2QRG4|H2QRG4_PANTR Interferon regulatory factor OS=Pan troglodytes GN=IRF1 PE=2 SV=1<br />MPITRMRMRPWLEMQINSNQIPGLIWINKEEMIFQIPWKHAAKHGWDINKDACLFRSWAI<br />HTGRYKAGEKEPDPKTWKANFRCAMNSLPDIEEVKDQSRNKGSSAVRVYRMLPPLTKNQR<br />KERKSKSSRDAKSKAKRKSCGDSSPDTFSDGLSSSTLPDDHSSYTVPGYMQDLEVERALT<br />PALSPCAVSSTLPDWHIPVEVVPDSTSDLYNFQVSPMPSTSEATTDEDEEGKLPEDIMKL<br />LEQSEWQPTNVDGKGYLLNEPGVQPTSVYGDFSCKEEPEIDSPGGDIGLSLQRVFTDLKN<br />MDATWLDSLLTPVRLPSIQAIPCAP</b><br /><br />Do I need to compare the rest of the promoters?Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-3434311642468417952015-11-02T14:41:42.585-05:002015-11-02T14:41:42.585-05:00Dazz
Your idea was very creative. If we stop the ...Dazz<br />Your idea was very creative. If we stop the debate and just do the science the discovery is about asking a question any coming up with a hypothesis. The titin differences may be testable and if so we can learn a lot about evolution. Hopefully you can see now that getting a testable final cause like design vs natural selection neutral theory etc is very difficult. My point is that there are lots of Science to do between those points and fossil records and gene data. I hope you can also see that if come up with a premature answer it can stop the science because you start restricting the possible solutions in your mind.Bill Colehttps://www.blogger.com/profile/06642212549806694659noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-29037921419904678602015-11-02T13:53:47.499-05:002015-11-02T13:53:47.499-05:00BTW, I don't know if the differences in the Ti...BTW, I don't know if the differences in the Titin are really due to mutations in regulatory genes or the TTN gene itslef, or both. The point is that there's nothing special about it that I can see. Still a 99% match with chimps, so...Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.comtag:blogger.com,1999:blog-37148773.post-8775516050262979232015-11-02T13:50:41.407-05:002015-11-02T13:50:41.407-05:00What regulatory gene?
I don't know even if it...<i>What regulatory gene?</i><br /><br />I don't know even if it's known. But it doesn't matter. The 99% match across the board is consistent with neutral variation and you keep ignoring that.<br /><br />You are again asking for an extremely detailed piece of evidence while you don't do that for other theories like gravity. If I ask you if the formation of the solar system is consistent with gravity/accretion, do you need to know what particles of the original nebula formed Saturn's rings to confirm the theory?Dazzhttps://www.blogger.com/profile/07619622297229101066noreply@blogger.com