Posted on 08/07/2007 9:30:37 AM PDT by GodGunsGuts
RIVERSIDE, Calif. A research team, including UC Riverside biologists, has found experimental evidence that supports a controversial theory of genetic conflict in the reproduction of those animals that support their developing offspring through a placenta.
The conflict has been likened to a battle of the sexes or an arms race at the molecular level between mothers and fathers. At stake: the fetuss growth rate and how much that costs the nutrient-supplying mother.
The new research supports the idea of a genetic arms race going on between a live-bearing mother and her offspring, assisted by the growth-promoting genes of the father...
(Excerpt) Read more at eurekalert.org ...
No, it is not. This is your question.
Why is the Vitamin C synthase gene broken in the exact same place in humans and apes?
"Exact same place" means "exact same place", not "throughout".
BTW- There are 5 codons that are exact: 6 7 12 15 16
Because females do not give that signal. They give the opposite signal. It is tied to the sex of the provider and it is the sex gene that determines sex.
Yes your right. 12/17 were “hot spots”. Sorry for the mistake.
To your satisfaction.
It was not the sequence that was important. It was the fact that the point where apes have a deletion is a point that is often mutated.
Every point in the genome is often mutated when one looks at enough species. The interesting part is the similarity AND the differences, not just at this one data point, but in all genes of the genome, pseudogenes, and ERV’s. The differences are more pronounced in unrelated species, the similarities are apparent in closely related species.
Wrong again. Making another baseless claim won't get you anywhere.
the best evidence suggests
You made the claim about MDRTB and cannot provide evidence to further your BS about MDRTB so you dance around having to provide proof by making the same baseless claim of ALL life.....nice tactic in Absurdistan. For some strange reason, I doubt you're scientifically qualified to look at the "evidence" let alone scientifically qualified to determine what evidence is "the best"...let along having a scientific understanding of what that "best evidence" "suggests."
PROVE IT.
Back up your BS for a change.
Of course humans and chimps are cousins.
But that has nothing to do with your cheap shot.
==Wrong again. Making another baseless claim won’t get you anywhere
Inheritance of acquired characteristics and Darwin’s ToE (RM+NS) cannot be true at the same time. If you can’t see that then their is something wrong with your knowledge base, your brain, or both.
==Did the new strains of Multi-Drug Resistant Tuberculosis evolve, or were they newly created? They didn’t exist before, so I think it’s one or the other.
Like I said, I can’t find anything that specifically deals with MDRTB, but there is a growing body of evidence that suggests that organisms are pre-programmed to survive via mechanisms that fly in the face of Darwinian evolution, i.e. non-random, directed mutations. This kind of evidence (pre-programing/front loading) is predicted by Creation Science/ID. And the only way for evolutionists to even have a chance of explaining this and still remain evolutionists is to fall back on Lamarckian evolution (which I predict they will begin to do in fairly short order). Read the following to get a flavor of what I’m talking about—GGG
Cheap shot? It must be your sense of guilt, since you have confirmed my statement which you claimed a "cheap shot." Which was --- Not for Darwinists, chimps are our cousins.
My comment was due to the fact that the person who prompted my comment dodged a perfectly legitimate test of his claim that Darwinism was predictive. He chose to bring in religious terms. I merely told him he was wrong to bring in those terms. Blasphemy is not a term which is addressed by Darwinism, but, according to him, predicting the result of a cross species is. So what is the predicted result?
Not for Darwinists...
That was the cheap shot. Show me a "Darwinist" who has attempted a chimp/human hybrid.
Do you really understand the word "predict"?
That's probably a good idea. As you have probably noticed by now, the person you're trying to have a conversation with will continue to miss the point (or pretend to) until the cows come home. He's really, really fond of lawyerly word fiddling in order to try to maintain a lost argument or an incorrect claim, like the way he's trying to rescue his mistake about "sex determination" by repeatedly blustering about how the active gene is from the father. You know and I know that this still doesn't make it "sex determination", and I doubt anyone else on the thread is having any trouble seeing through his sophistry, but he'll continue for the rest of his life to pretend that *he's* not the one who made a mistake, *you're* just not understanding his brilliant argument... He's been that way for years. You'll never get around his inability to admit even the most obvious of error. Your time is better spent arguing with housecats.
He's also not above coming back literally years later and trying to declare victory when actually he was thoroughly rebutted on the original thread. He actually did that today on this thread, about a discussion that took place FOUR YEARS AGO. Note his post #164, where he claims that he "did an analysis of the vitamin C mutations quite a while ago". Well actually, he just made some vague implications about the fact that some sites had changed more than others. He didn't actually do anything that would rise to an "analysis". If you want actual analysis of that gene sequence (and examination of his inneundo about it) see here, here, and here.
In post #164 above he further makes this amazing claim: "A certain individual, who shall remain unnamed, attempted a rebuttal. But he couldn't count so I have left it to hang splendedly [sic] for years." Actually, that "unnamed individual" would be me. And I did more than "attempt a rebuttal", I made a complete and thorough rebuttal to his goofy implications about how there seems to be something unseemly about the number or clustering of the mutations in the GLO gene. Here is that rebuttal (original post here):
[The poster known as Mr. LLLICHY wrote:] Here is that Vitamin C dataWithin minutes after posting that I noticed that I had made the same minor mistake you recently made when comparing the human and chimp sequences, and I quickly followed that post with the following:After discovering this same data on another thread along with more discussion than has appeared here (I've taken the liberty of pinging the participants of that discussion), I see what the "mystery" is supposed to be -- it's supposed be why did some sites have multiple mutations while (small) stretches of other sites had none? In other words, why do the mutations appear clustered?
(You know, it would really help if people explained their points and questions in more detail, instead of leaving people to guess what the poster was thinking...)
[LLLICHY wrote:] "U238" that decays thrice, pretty good trick when there is "U238" that does not decay at all in 50,000,000 years.
Actually, no site had mutations "thrice". Three different bases at a given site is only *two* mutations (one original base, plus two mutations from it to something else).
Here's the "mutation map" from the actual DNA data:
--1-12--1-1-1-1--------1112112--1---1-11-1--------1 ALL/nNo mutations ("-") in about half the sites, one mutation at several (17) sites, two mutations at three sites.The first thing to keep in mind that random processes tend to "cluster" more than people expect anyway. People expect "randomness" to "spread out" somewhat evenly, but instead it's usually more "clumped", for statistical reasons that would be a diversion to go into right now. So "that looks uneven" isn't always a good indication that something truly is non-random.
If you don't believe me on that, I wrote a program which made 23 mutations totally at random on a 51-site sequence, then repeated the process to see what different random outcomes would look like:
10 X$=STRING$(51,"-") 20 FOR I=1 TO 23 30 J%=INT(RND*51)+1 40 C$=MID$(X$,J%,1) 50 IF C$="-" THEN MID$(X$,J%,1)="1" ELSE MID$(X$,J%,1)=CHR$(ASC(C$)+1) 60 NEXT I 70 PRINT X$ 80 GOTO 10Yeah, it's BASIC, so sue me. Here's a typical screenful of the results:-21---1---2---111----2-----2-1121-------1---1--11-1 -1--1--21-11---1-1--1-1---1----1---21-11111---11--- 3-11---3-----1-----11-2-1---1--1----3--2---1--1---- ---1-1--22--1-1--2-2111--1-1111---1------1-------1- ---32----1-11-1-----1---2-231----1------1-----11--1 ----2---21--1---4----1-------------11-1--111-11-211 11--1-1---1-----1--1------1----3111--1----111-2-1-2 1112---1-3-1----1-1-----1-1------121--111-------1-1 -111121--1----1----1-1-1-1-11-2---1-1-------1-111-- -----------11-1---11-11--------21----12211--1---131 --1-211-1-1----21--11-1-2----1--1----11---11-----11 12---1-13------------2---21-21---11-1-1-1--2------- -----2-1---1-1----21--11-11-1---111-1--111-----2--1 -----1-----1-1-1-1---1-2----11-21-11--1-111---1-21- ---11--1-1-122-1-1-1--1-----2-1-1-1-------1-1---111 --2--11----2--1---12-2----1-1---1-1--1--12----1-1-1 -111-1-----1-1----------1-21111--1-2-11-11-1----11- 11-1--211-1221-----1--1-----11--1-2-1----------11-- -----1-12-11---2-1---11--1-2--1----11---111-1----11 11----1--12---12----1---31---1-11----2--1-11-1----- ---1--111-1--1-1-111----1-21----1-1-3---1------2--1 -2-11----1-1------1------2-1-1--111-111-1-1----1111 1--1--1-1---1-111111--2--1-1------112----2---11----Notice how oddly "clustered" most of them look, including one run which left a 13-site stretch "absolutely untouched", contrary to intuition (while having *4* mutations at a single site!)Frankly, I don't see anything in the real-life DNA mutation map which looks any different from these truly random runs. Random events tend to cluster more than people expect. That solves the "mystery" right there.
Also, there may be a selection factor -- the GLO gene is a *lot* bigger than this. One has to wonder if this small 51-bp section was presented just because it was the one that looked "least random". That would be a no-no, since one can always hand-select the most deviant subset out of larger sample in order to artificially skew the picture.
However, since there are some interesting evolutionary observations to be made, let's look at that DNA data again, slightly rearranged:
TAC CCC GTG GAG GTG CGC TTC ACT CGG GCG GAC GAC ATC CTG CTG AGC CCC PIG TAC CCC GTG GAG GTA CGC TTC ACT CGC GGG GAC GAC ATC CTG CTG AGC CCC BOS TAC CCC GTA GAG GTG CGC TTC ACC CGA GGC GAT GAC ATT CTG CTG AGC CCC RAT TAC CCC GTG GAG GTG CGC TTC ACC CGA GGT GAT GAC ATC CTG CTG AGC CCG MOUSE TAC CCT GTG GGG GTG CGC TTC ACC CGG GGG GAC GAC ATC CTG CTG AGC CCC GUIN PIG TAC CTG GTG GGG GTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC HUMAN TAC CTG GTG GGG CTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC CHIMPANZEE TAC CCG GTG GGG GTG CGC TTC ACC CAG AG* GAT GAC GTC CTA CTG AGC CCC ORANGUTAN TAA CCG GTG GGG GTG CGC TTC ACC CAA GG* GAT GAC ATC ATA CTG AGC CCC MACAQUEHere I've put spaces between codons, and clustered the closely-related species together: pig/cow as ungulates, rat/mouse for their obvious relationship, guinea pig right below them but separated because of the pseudogene nature of its GLO gene, then primates all in a group, with man's closest relative, the chimp, immediately below him, followed by the more distant orangutan, and the even more distant macaque. Also note that the top four have "working" GLO genes, and the bottom five have "broken" GLO pseudogenes.First, let's consider just the four species with working GLO genes. Evolution predicts that even over large periods of time, these genes will be "highly conserved", with natural selection weeding out mutations that could "break" the gene. Note that the mutations will still have occurred in individuals of the population, but natural selection will "discourage" that mutation from spreading into the general population.
And before we go any further, let's talk about the "universal genetic code". In all mammals (indeed, in almost all living organisms), each triplet of DNA sites cause a particular amino acid to be formed. The mapping of triplets (called "codons") to amino acids is as follows:
Second Position of Codon T C A G F
i
r
s
t
P
o
s
i
t
i
o
nT
TTT Phe [F] TTC Phe [F] TTA Leu [L] TTG Leu [L]
TCT Ser [S] TCC Ser [S] TCA Ser [S] TCG Ser [S]
TAT Tyr [Y] TAC Tyr [Y] TAA Ter [end] TAG Ter [end]
TGT Cys [C] TGC Cys [C] TGA Ter [end] TGG Trp [W]
T C A G T
h
i
r
d
P
o
s
i
t
i
o
nC
CTT Leu [L] CTC Leu [L] CTA Leu [L] CTG Leu [L]
CCT Pro [P] CCC Pro [P] CCA Pro [P] CCG Pro [P]
CAT His [H] CAC His [H] CAA Gln [Q] CAG Gln [Q]
CGT Arg [R] CGC Arg [R] CGA Arg [R] CGG Arg [R]
T C A G A
ATT Ile [I] ATC Ile [I] ATA Ile [I] ATG Met [M]
ACT Thr [T] ACC Thr [T] ACA Thr [T] ACG Thr [T]
AAT Asn [N] AAC Asn [N] AAA Lys [K] AAG Lys [K]
AGT Ser [S] AGC Ser [S] AGA Arg [R] AGG Arg [R]
T C A G G
GTT Val [V] GTC Val [V] GTA Val [V] GTG Val [V]
GCT Ala [A] GCC Ala [A] GCA Ala [A] GCG Ala [A]
GAT Asp [D] GAC Asp [D] GAA Glu [E] GAG Glu [E]
GGT Gly [G] GGC Gly [G] GGA Gly [G] GGG Gly [G]
T C A G (The above table imported from http://psyche.uthct.edu/shaun/SBlack/geneticd.html, which also has a nice introduction to the genetic code.)
Another version of the same table with nifty Java features and DNA database lookups can be found here.
The thing which is most relevant to the following discussion is the fact that most of the genetic codes are "redundant" -- more than one codon (triplet) encodes to exactly the same amino acid. This means that even in genes which are required for the organism, certain basepair mutations make absolutely no difference if the change is from one codon which maps into amino acid X to another codon which still maps into amino acid X. (This fact allows certain kinds of evolutionary "tracers" to be "read" from the DNA, as described here).
Now back to our DNA data. The redundancy in the genetic code means that some basepair sites will have more "degrees of freedom" than others (i.e., ways in which they can mutate without disrupting the gene's biological function in any way). Let's look at the four species with working GLO genes again:
TAC CCC GTG GAG GTG CGC TTC ACT CGG GCG GAC GAC ATC CTG CTG AGC CCC PIG TAC CCC GTG GAG GTA CGC TTC ACT CGC GGG GAC GAC ATC CTG CTG AGC CCC BOS TAC CCC GTA GAG GTG CGC TTC ACC CGA GGC GAT GAC ATT CTG CTG AGC CCC RAT TAC CCC GTG GAG GTG CGC TTC ACC CGA GGT GAT GAC ATC CTG CTG AGC CCG MOUSE T T T A T A T T T A T C C T T T T T T T T A A A A A C A A A A A G C G G G G G C C C --- --- --1 --- --1 --- --- --1 --2 -12 --1 --- --1 --- --- --- --1Under each site of the mouse DNA, I've listed the "alternative" bases which could be be substituted for the mouse base at that site WITHOUT ALTERING THE GENE'S FUNCTION (because of genetic code redundancy). And under that I show the "mutation map" of just those four species.Note that most of the "alternative" bases are in the third base of each codon, *and* that this is where all but one of the mutations have appeared. This is because these were the sites which were "free" to mutate in the way they did, because the mutation was genetically neutral. That doesn't mean that the first and second sites of each codon were immune from mutation, it's just that when mutations did occur at those sites, natural selection weeded them out quickly because they most likely "broke" the GLO gene for the individuals which received that mutuation. What we see above is the results after natural selection has already "filtered" the undesirable mutations and left the ones which "do no harm".
Additionally, the two sites which have mutated twice (i.e. have a "2" in the mutation map) are ones which had more "allowable" mutations. Also note that the sites which had the fewest allowable alternatives (only one alternate letter allowed) didn't have any mutations fix at those sites, which is unsurprising since a "safe" mutation would be less likely to occur there versus a site that "allowed" two or three alternatives.
All this is as predicted by evolutionary theory, you'll note.
It also explains the one anomoly of the original mutation map, which is that the mutation counts do tend to be higher at the third base of a codon.
However... What about the one exception? The pig DNA has had one mutation at a site which does not encode to exactly the same amino acid (which is the case for *all* the other ones). In the pig DNA, the GGG codon (mapping to Glycine) has changed to a GCG codon (mapping to Alanine). What's up with that? Well, one of two things. First and most likely, just as base values in codons have a built-in redundancy, so do the amino acids which make up the proteins which result from the DNA templates. In other words, certain amino acids can be substituted for other ones at some sites in given proteins without making any functional difference. (This "protein functional redundancy" also has implications for "evolutionary tracer" analysis, see here.) That may well be the case for Alanine versus Glycine in the GLO protein, but I'm not enough of a biochemist to be able to say. The other option is that it *does* make some difference in the function of the pig GLO protein, but not enough to "break" the vitamin-C synthesis (as proven by the fact that pigs *can* synthesize vitamin C). So one way or another, it's not a deal-breaker even though pig GLO will not be 100% identical to cow/mouse/rat GLO. It's yet another "allowable" mutation.
More interesting evolutionary observations: The number of mutational differences between pig/cow is 3, the number between mouse/rat is 4, and the difference between rat/cow is 7 -- all roughly as one would expect from the evolutionary relatedness of these animals (cows/pigs and rats/mice are each closer to each other than the rodents are to the ungulates).
Now let's take a close look at the guinea pig:
TAC CCT GTG GGG GTG CGC TTC ACC CGG GGG GAC GAC ATC CTG CTG AGC CCC GUIN PIG --- --1 --- -1- --- --- --- --- --1 --1 --1 --- --- --- --- --- ---The "mutation map" under the guinea pig DNA is compared to the mouse DNA. Fascinating: Note that four of the five mutations are in the third base of a codon, *and* are of the type "allowed" by the genetic code redundancy. This indicates strongly that most of the evolutionary divergence between guinea pigs and mice likely occurred while the guinea pig's ancestors still had a working GLO gene. This is the sort of prediction implied by the evolutionary theory which could be cross-checked by further research of various types, and if verified, would be yet further confirmation that evolutionary theory is likely correct. So far, evolutionary theory has been subjected to literally countless tests like this, large and small, and the vast majority of results have confirmed the evolutionary prediction. This track record is hard to explain if evolution is an invalid theory, as some assert...Finally, let's look over the primate DNA and mutation map (relative to each other):
TAC CTG GTG GGG GTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC HUMAN TAC CTG GTG GGG CTA CGC TTC ACC TGG AG* GAT GAC ATC CTA CTG AGC CCC CHIMPANZEE TAC CCG GTG GGG GTG CGC TTC ACC CAG AG* GAT GAC GTC CTA CTG AGC CCC ORANGUTAN TAA CCG GTG GGG GTG CGC TTC ACC CAA GG* GAT GAC ATC ATA CTG AGC CCC MACAQUE --1 -1- --- --- 1-1 --- --- --- 111 1-- --- --- 1-- 1-- --- --- ---Evolutionary theory predicts that because the GLO gene is "broken" in primates (i.e. is a pseudogene), mutations in it are highly likely to be neutral (i.e., make no difference, since it can't get much more broken), and thus mutations are just as likely to accumulate at any site as any other. Is that what we see? Yup. There's no obvious pattern to the mutations between primates in the above mutation map, and unlike the pig/cow/mouse/rat mutation map, the mutations aren't predominantly at the "safer" third base of a codon, nor of a type that would be "safe". In fact, one base has vanished entirely, but no biggie, the gene's already broken.Also, although primates share a more recent common ancestor than cows/pigs/mice/rats, note that they've already racked up almost as many relative mutations as the cow/pig/mouse/rat DNA. This too is just as evolutionary theory predicts, because many mutations in a functional gene (GLO in this case) will be "non-safe" and weeded out by natural selection, making for a slower mutation fixation rate overall than in a pseudogene (as GLO is in primates) where natural selection doesn't "care" about the vast majority of mutations since *most* are neutral. So pseudogenes accumulate mutations faster than functional genes (even though rate of mutation *occurence* in both are likely the same).
Finally, note that there are ZERO mutational differences between the human DNA and the chimpanzee DNA, our nearest living relative.
I also see some interesting implications in the DNA sequences concerning which specific mutation fixed during what branch of the common-descent evolutionary tree for all the species represented, but reconstructing that would not only take another couple hours, at least, but would be a major bear to code in HTML, since I'd have to draw trees with annotations on the nodes... Bleugh.
In any case, I hope I've clarified some of the methods by which biologists find countless confirmations of evolution in DNA data. This is just a "baby" example, and to be more statistically valid would have to be done over much vaster sections of DNA sequences, but my intent was to demonstrate some of the concepts.
And if such a small amount of DNA as this can make small confirmations of evolutionary predictions, imagine the amount of confirmation from billion-basepair DNA data from each species compared across thousands of species... The amount of confirmatory discoveries for evolution from DNA analysis has already been vast, and promises to only grow in the future. For an overview of some of the different lines of evidence being studied, see The Journal of Molecular Evolution -- abstracts of all articles, current and back issues, can be browsed free online.
Finally, note that there are ZERO mutational differences between the human DNA and the chimpanzee DNA, our nearest living relative.You'll note that this minor miscount didn't affect the validity of my rebuttal -- none of my actual rebuttal relied on that count, the rebuttal is just as valid with the correction included.Grrr... Okay, make that "one". At this time of morning my tired eyes couldn't see the difference between a "C" and a "G" the first time around.
This is why the poster you're finding so aggravating never even attempted a defense of his original post, nor had he contested the validity of my rebuttal at the time. It's actually quite unlike him to just drop a topic like that after being rebutted. Instead all he could manage was a small post pointing out another small miscount (again my eyes, like yours, had had trouble visually spotting the "C" versus "G"), and to point out an implied mutation that was beyond the scope of my original rebuttal (because it relied on phylogeny reconstructions that many on the thread would have objected to as contentious). Neither observation affected the validity of my rebuttal -- again, it's just as valid with the minor miscounts in the tallies corrected, nor at the time did he attempt to argue that the C/G oversights were a blow to my actual rebuttal, because of course they weren't.
And yet, incredibly, *now* (four years later) he tries to claim victory and writes (in post #164): "But he couldn't count so I have left it to hang splendedly for years.", as if *now* he wants to imply that the minor miscounts somehow invalidate all the ways in which I pointed out the flaws in his claims and innuendo across multiple posts (linked above), even though he didn't contest the rebuttal at the time. Sheesh! I suppose that in another four years on some unrelated thread he'll be declaring victory over you with regards to his "sex determination" mistake.
Sorry, but a thorough rebuttal doesn't get any less valid with age, nor does a minor miscount invalidate all the points it makes and the evidence is provides and the errors it identifies in someone's posts, nor can someone get away with making misrepresentations about it years later in the hopes that no one will notice and call them on it...
It takes a lot of gall to try to misrepresent a past discussion that badly. Heck, it takes a lot of obsession to even bring it up four years later. I must have really hit a nerve.
He ends his recent post with, "there are at least 3 mutations at that point(there are only 4 bases so three mutations run the gamut). It is a hot spot." Um, no. First, "three mutations run the gamut" is wrong, because he's including a deletion in his count. He's overlooking the fact that no genome shows an "A" nucleotide in that spot, which if it had occurred would have been *four* mutations, more than his claims of three being "the gamut". OOPS! Hey, what was that about NOT BEING ABLE TO COUNT? Hoist on his own petard! Irony is so ironic!
Second, one could play word games and try to assert that it's a "hot spot" in the common-language sense that it's where more mutations have managed to fix in the genomes being discussed relative to other spots, but (for all the reasons I gave in my original rebuttal, included above), that doesn't demonstrate that this is actually a "hot spot" in the sense that it's necessarily a spot which undergoes a higher mutation rate, which is how biologists almost exclusively use the term (many examples). Fixation rate is not mutation rate. Again, as I pointed out in my original rebuttal, a) some spots are going to have a "surprising" number of mutations pile up EVEN IN A PURELY RANDOM SCENARIO via the way that ordinary laws of statistics operate (which means that you can't draw any "hot spot" conclusion just from the fact that some spot has accumulated a paltry 3-4 mutations over a few million years), and b) the third basepair in a codon is naturally more "free" to fix mutations than positions one and two in the codon, so higher fixation rates for mutations in the third position of a codon is *not* itself a valid reason for concluding that the locus has a higher *mutation* rate (i.e. is a true "hot spot"), because natural selection acts as a *filter* which *retains* more mutations occurring at those spots relative to other codon positions.
I was quite clear about all this in my original rebuttal -- it's a shame he didn't understand it at all, which is why he is now falsely claiming "victory" and rashly repeating his fallacious claims about how his genome snippet is enough to identify "hot spots" long after he has been presented with a thorough rebuttal that he has been unable to identify any substantive flaw in. Sad, really.
Finally, he is making the elementary mistake of considering "random" and "having hot spots" as somehow mutually exclusive terms -- note how he used his (fallaciously employed) sequence non-analysis which he incorrectly believed was enough to demonstrate "hot spots" in order to "disagree" with your correct assertion that mutations have time and again been found to occur randomly. Ironically, he shoots himself in the foot with his own first example, that of "7" appearing as a total of two thrown dice more often than "2". To anyone who understands how dice work, this actually undercuts the points he's been trying to make and reinforces yours, since no one is foolish enough to assert that the higher frequency of "7" appearing on a pair of thrown dice is due to an invisible hand altering the roll of each dice throw because it "likes" the number seven, instead it's just a natural consequence of the unguided dynamics of *random* dice rolls. The fact that some totals appear more often than others (because there are more combinatorial ways in which they can occur during *random* pairings) is no argument against the correct claim that the outcome of dice rolls are *random* and guided mechanically by the laws of statistics and physics rather than by an unseen "guiding hand". Hoist on his own petard *again*.
And if anyone is wondering why I refer to him by a nickname in that rebuttal and talked about his post while directing my reply to someone else intead of him (and why I don't ping him to *this* post), you'll find the answer on that same prior thread in a big back-and-forth exchange between posts #468 and #1508-- short form is that he couldn't stand to see my rebuttals anymore and demanded that I not ping him to them. So I don't.
Real science is so hard! Lets all go to the mall.
The individual still can't count(plus GTA <> CTA so "zero difference" is not zero). Three bases at a position denotes at least 2 mutations. No letter at the same spot adds another mutation. That is three. The gamut is in reference to the fact that 3 mutations not involving a deletion and only substitutions are all that can be determined for that particular locus. We have hit that number despite his miscount "Actually, no site had mutations "thrice". Three different bases at a given site is only *two* mutations (one original base, plus two mutations from it to something else). " Plus the deletion hides the possibility of the other base prior to the deletion. And the composite picture of the mutations involves countless generations of a sequence not just samples of a random sequence containing 23 "hits". Consolidate the sequences and see what you get.
Finally, the pseudogenes have no Darwinian reason to have any section conserved. Subsequent experiments show that "junk DNA" can be highly conserved. That was my point about the vitamin C pseudogene.
Not exactly true. The Communists under Marx and then Lenin began as Darwinists, deviated into Lamarckism under Stalin/Lysenko (while Darwinism was on the wane and Lamarck was quite in vogue, I might add) , and then returned Darwin to his rightful place of Communist honor after Stalin died.
Do you know why yet? Do you still think it is sex determination? Willing to take a guess at the Lyger Tigon question and show us the brilliant predictive power of creation science?
All the apes listed have pseudogenes, the other species have functioning Vitamin C Synthase genes. As long as your talking about genetic conservation, did you know that pseudogenes and genes have measurably different mutation rates?
In other words if one measures the difference in the pseudogene shared in common between humans and gorillas and the genes shared in common you will find that the pseudogenes are not as conserved; and the predicted rate of divergence between pseudogens and genes will both converge on the same predicted date for having a common ancestor. Do the same comparing the rate of divergence between the pseudogenes and genes shared in common with humans and orangutans and it will also converge, but at a later date. Chimps would come in at an earlier date, reflecting our more recent common ancestry.
So yes, there is no “Darwinian” (natural selection) reason for the pseudogenes to be conserved in humans, chimps, and gorillas; they mutate at the predicted neutral mutation rate and all accurately show the predicted time of divergence. There is also no reason in natural selection for the genes to be so highly homologous in closely related species and so different in unrelated species, the protein they code for are often indistinguishable in any functional parameters, the only theory that explains it is common descent.
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