No, he's discussing the biology.
Despite the similarities, it is a fact that the ape is anthropoid, not human, the gap between them being precisely what distinguishes the beast from man. a fact that evolutionists must deal with is that there are no evolutionists who are apes.
Wrong again: You are an ape. Humans *are* ape. Apes of the human variety. Just as tigers are cats -- cats of of the tiger variety. It's not either/or, we are still apes, just as we are still mammals, still vertebrates, still eukaryotes, etc.
If you disagree -- on *biological* grounds -- feel free to name a set of traits that distinguish the ape group from other animals, which humans do not also exhibit.
Accepting evolution as true,
It is.
the common ancestor of man and ape is so remote that no postive trail can be discerned.
ROFL!!! You really *don't* know any biology, do you? Or are you just lying, like so many other anti-evolutionists?
"No positive trail can be discerned", eh? Really? Little do you know how little you know:
Or how about:Background: Retroviruses reproduce by entering a cell of a host (like, say, a human), then embedding their own viral DNA into the cell's own DNA, which has the effect of adding a "recipe" for manufacturing more viruses to the cell's "instruction book". The cell then follows those instructions because it has no reason (or way) to "mistrust" the DNA instructions it contains. So the virus has converted the cell into a virus factory, and the new viruses leave the cell, and go find more cells to infect, etc.
However, every once in a while a virus's invasion plans don't function exactly as they should, and the virus's DNA (or portions of it) gets embedded into the cell's DNA in a "broken" manner. It's stuck into there, becoming part of the cell's DNA, but it's unable to produce new viruses. So there it remains, embedded in the DNA. If this happens in a regular body cell, it just remains there for life as a "fossil" of the past infection and goes to the grave with the individual it's stuck in. All of us almost certainly contain countless such relics of the past viral infections we've fought off.
However... By chance this sometimes happens to a special cell in the body, a gametocyte cell that's one of the ones responsible for making sperm in males and egg cells in females, and if so subsequent sperm/eggs produced by that cell will contain copies of the "fossil" virus, since now it's just a portion of the entire DNA package of the cell. And once in a blue moon such a sperm or egg is lucky enough to be one of the few which participate in fertilization and are used to produce a child -- who will now inherit copies of the "fossilized" viral DNA in every cell of his/her body, since all are copied from the DNA of the original modified sperm/egg.
So now the "fossilized" viral DNA sequence will be passed on to *their* children, and their children's children, and so on. Through a process called neutral genetic drift, given enough time (it happens faster in smaller populations than large) the "fossil" viral DNA will either be flushed out of the population eventually, *or* by luck of the draw end up in every member of the population X generations down the road. It all depends on a roll of the genetic dice.
Due to the hurdles, "fossil" retroviral DNA strings (known by the technical name of "endogenous retroviruses") don't end up ubiquitous in a species very often, but it provably *does* happen. In fact, the Human DNA project has identified literally *thousands* of such fossilized "relics" of long-ago ancestral infections in the human DNA.
And several features of these DNA relics can be used to demonstrate common descent, including their *location*. The reason is that retroviruses aren't very picky about where their DNA gets inserted into the host DNA. Even in an infection in a *single* individual, each infected cell has the retroviral DNA inserted into different locations than any other cell. Because the host DNA is so enormous (billions of basepairs in humans, for example), the odds of any retroviral insertion event matching the insertion location of any other insertion event are astronomically low. The only plausible mechanism by which two individuals could have retroviral DNA inserted into exactly the same location in their respective DNAs is if they inherited copies of that DNA from the same source -- a common ancestor.
Thus, shared endogenous retroviruses between, say, ape and man is almost irrefutable evidence that they descended from a common ancestor. *Unless* you want to suggest that they were created separately, and then a virus they were both susceptible to infected both a man and an ape in EXACTLY the same location in their DNAs (the odds of such a match by luck are literally on the order of 1,000,000,000,000 to 1...), *and* that the infections both happened in their gametocyte cells (combined odds on the order of 1,000,000 to 1) *and* that the one particular affected gametocyte is the one which produces the egg or sperm which is destined to produce an offspring (*HUGE* odds against), and *then* the resulting modified genome of the offspring becomes "fixed" in each respective population (1 out of population_size^squared)...
Then repeat that for *each* shared endogenous retrovirus (there are many) you'd like to claim was acquired independently and *not* from a shared ancestor...
Finally, you'd have to explain why, for say species A, B, and C, the pattern of shared same-location retroviruses is always *nested*, never *overlapped*. For example, all three will share some retroviruses, then A and B will both share several more, but if so then B *never* shares one with C that A doesn't also have (or at least remnants of).
In your "shared infection due to genetic similarities" suggestion, even leaving aside the near statistical impossibility of the infections leaving genetic "scars" in *exactly* the same locations in independent infections, one would expect to find cases of three species X, Y, and Z, where the degree of similarity was such that Y was "between" X and Z on some similarity scale, causing the same disease to befall X and Y but not Z, and another disease to affect Y and Z but not X. And yet, we don't find this in genetic markers. The markers are found in nested sequence, which is precisely what we would expect to see in cases of inheritance from common ancestry.
Here, for example, is an ancestry tree showing the pattern of shared same-location endogenous retroviruses of type HERV-K among primates:
This is just a partial list for illustration purposes -- there are many more.
Each labeled arrow on the chart shows an ERV shared in common by all the branches to the right, and *not* the branches that are "left-and-down". This is the pattern that common descent would make. And common descent is the *only* plausible explanation for it. Furthermore, similar findings tie together larger mammal groups into successively larger "superfamilies" of creatures all descended from a common ancestor.
Any presumption of independent acquisition is literally astronomically unlikely. And "God chose to put broken relics of viral infections that never actually happened into our DNA and line them up only in patterns that would provide incredibly strong evidence of common descent which hadn't actually happened" just strains credulity (not to mention would raise troubling questions about God's motives for such a misleading act).
Once again, the evidence for common descent -- as opposed to any other conceivable alternative explanation -- is clear and overwhelming.
Wait, want more? Endogenous retroviruses are just *one* type of genetic "tag" that makes perfect sense evolutionary and *no* sense under any other scenario. In addition to ERV's, there are also similar arguments for the patterns across species of Protein functional redundancies, DNA coding redundancies, shared Processed pseudogenes, shared Transposons (including *several* independent varieties, such as SINEs and LINEs), shared redundant pseudogenes, etc. etc. Here, for example, is a small map of shared SINE events among various mammal groups:
Like ERV's, any scenario which suggests that these shared DNA features were acquired separately strains the laws of probability beyond the breaking point, but they make perfect sense from an evolutionary common-descent scenario. In the above data, it is clear that the only logical conclusion is that, for example, the cetaceans, hippos, and ruminants shared a common ancestor, in which SINE events B and C entered its DNA and then was passed on to its descendants, yet this occurred after the point in time where an earlier common ancestor had given rise both to that species, and to the lineage which later became pigs.
And this pattern (giving the *same* results) is repeated over and over and over again when various kinds of molecular evidence from DNA is examined in detail.
The molecular evidence for evolution and common descent is overwhelming. The only alternative is for creationists to deny the obvious and say, "well maybe God decided to set up all DNA in *only* ways that were consistent with an evolutionary result even though He'd have a lot more options open to him, even including parts which by every measure are useless and exactly mimic copy errors, ancient infections, stutters, and other garbage inherited from nonexistent shared ancestors"...
Humans have 23 pairs of chromosomes ---chimps and gorillas have 24 pairs. How many pairs of chromosomes did the "common ancestor" have? Was it 23 or 24 pairs? How do you "evolve" missing or added chromosomes ---that would happen all at one time.And:The common ancestor had 24 chromosomes.
If you look at the gene sequences, you'll find that Chromosome 2 in humans is pretty much just 2 shorter chimpanzee chromosomes pasted end-to-end, with perhaps a slight bit of lost overlap:
(H=Human, C=Chimpanzee, G=Gorilla, O=Orangutan)
Somewhere along the line, after humans split off from the other great apes, or during the split itself, there was an accidental fusion of two chromosomes, end-to-end. Where there used to be 24 chromosomes, now there were 23, but containing the same total genes, so other than a "repackaging", the DNA "instructions" remained the same.
If a chimpanzee gives birth to a creature with 23 chromosomes, that offspring isn't going to be a well-formed chimpanzee able to survive well.
It is if the same genes are present, which they would be in the case of a chromosome fusion.
Evolve would imply the genetic material changes little by little --not some big loss of two chromosomes at once but I don't see how they'd go away gene by gene.
Tacking two chromosomes together end-to-end is not a "big loss" of genes, and it really is a "little by little" change in the total genetic code. It's just been "regrouped" a bit. Instead of coming in 24 "packages", it's now contained in 23, but the contents are the same.
So how, you might ask, would the chromosomes from the first 23-chromosome "fused" individual match up with the 24 chromosomes from its mate when it tried to produce offspring? Very well, thanks for asking. The "top half" of the new extra-long Chromosome 2 would adhere to the original chromosome (call it "2p") from which it was formed, and likewise for the "bottom half" which would adhere to the other original shorter chromosome (call it "2q"). In the picture above, imagine the two chimp chromosomes sliding over to "match up" against the human chromosome. The chimp chromosomes would end up butting ends with each other, or slightly overlapping in a "kink", but chromosomes have overcome worse mismatches (just consider the XY pair in every human male -- the X and the Y chromosome are *very* different in shape, length, and structure, but they still pair up).
In fact, the "rubbing ends" of the matched-up chimp chromosomes, adhering to the double-long human-type chromosome, would be more likely to become fused together themselves.
For studies in which recent chromosome fusions have been discovered and found not to cause infertility, see:
Chromosomal heterozygosity and fertility in house mice (Mus musculus domesticus) from Northern Italy. Hauffe HC, Searle JB Department of Zoology, University of Oxford, Oxford OX1 3PS, United Kingdom. hauffe@novanet.itIn that last reference, the Przewalski horse, which has 33 chromosomes, and the domestic horse, with 32 chromosomes (due to a fusion), are able to mate and produce fertile offspring.An observed chromosome fusion: Hereditas 1998;129(2):177-80 A new centric fusion translocation in cattle: rob (13;19). Molteni L, De Giovanni-Macchi A, Succi G, Cremonesi F, Stacchezzini S, Di Meo GP, Iannuzzi L Institute of Animal Husbandry, Faculty of Agricultural Science, Milan, Italy.
J Reprod Fertil 1979 Nov;57(2):363-75 Cytogenetics and reproduction of sheep with multiple centric fusions (Robertsonian translocations). Bruere AN, Ellis PM
J Reprod Fertil Suppl 1975 Oct;(23):356-70 Cytogenetic studies of three equine hybrids. Chandley AC, Short RV, Allen WR.
Meanwhile, the question may be asked, how do we know that the human Chromosome 2 is actually the result of a chromsome fusion at/since a common ancestor, and not simply a matter of "different design"?
Well, if two chromsomes accidentally merged, there should be molecular remnants of the original chromosomal structures (while a chromosome designed from scratch would have no need for such leftover "train-wreck" pieces).
Ends of chromosomes have characteristic DNA base-pair sequences called "telomeres". And there are indeed remnants of telomeres at the point of presumed fusion on human Chromosome 2 (i.e., where the two ancestral ape chromosomes merged end-to-end). If I may crib from a web page:
Telomeres in humans have been shown to consist of head to tail repeats of the bases 5'TTAGGG running toward the end of the chromosome. Furthermore, there is a characteristic pattern of the base pairs in what is called the pre-telomeric region, the region just before the telomere. When the vicinity of chromosome 2 where the fusion is expected to occur (based on comparison to chimp chromosomes 2p and 2q) is examined, we see first sequences that are characteristic of the pre-telomeric region, then a section of telomeric sequences, and then another section of pre-telomeric sequences. Furthermore, in the telomeric section, it is observed that there is a point where instead of being arranged head to tail, the telomeric repeats suddenly reverse direction - becoming (CCCTAA)3' instead of 5'(TTAGGG), and the second pre-telomeric section is also the reverse of the first telomeric section. This pattern is precisely as predicted by a telomere to telomere fusion of the chimpanzee (ancestor) 2p and 2q chromosomes, and in precisely the expected location. Note that the CCCTAA sequence is the reversed complement of TTAGGG (C pairs with G, and T pairs with A).Another piece of evidence is that if human Chromosome 2 had formed by chromosome fusion in an ancestor instead of being designed "as is", it should have evidence of 2 centromeres (the "pinched waist" in the picture above -- chromosomes have centromeres to aid in cell division). A "designed" chromosome would need only 1 centromere. An accidentally "merged" chromosome would show evidence of the 2 centromeres from the two chromosomes it merged from (one from each). And indeed, as documented in (Avarello R, Pedicini A, Caiulo A, Zuffardi O, Fraccaro M, Evidence for an ancestral alphoid domain on the long arm of human chromosome 2. Hum Genet 1992 May;89(2):247-9), the functional centromere found on human Chromosome 2 lines up with the centromere of the chimp 2p chromosome, while there are non-functional remnants of the chimp 2q centromere at the expected location on the human chromosome.As an aside, the next time some creationist claims that there is "no evidence" for common ancestry or evolution, keep in mind that the sort of detailed "detective story" discussed above is repeated literally COUNTLESS times in the ordinary pursuit of scientific research and examination of biological and other types of evidence. Common ancestry and evolution is confirmed in bit and little ways over and over and over again. It's not just something that a couple of whacky anti-religionists dream up out of thin air and promulgate for no reason, as the creationists would have you believe.
[The poster known as Mr. LLLICHY wrote:] Here is that Vitamin C dataAfter 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.
The "missing link" dilemma is a kind of caricatire of the facts, but the scarcity of intermediate forms requires a leap of faith.
Um, really? I don't see any "scarcity of intermediate forms" here -- quite the contrary:
Fossil Hominids: The Evidence for Human Evolution.
Where exactly is the "missing" transition in the following sequence? It looks pretty complete and gradual to me -- certainly there's no sudden "jump", no discontinuity, no pair between which a creationist would have any trouble dismissing such a small amount of change as "just microevolution", "just variation within a kind":
(The above is from 29 Evidences for Macroevolution -- Part 1: The Unique Universal Phylogenetic Tree)Figure 1.4.4. Fossil hominid skulls. Some of the figures have been modified for ease of comparison (only left-right mirroring or removal of a jawbone). (Images © 2000 Smithsonian Institution.)
- (A) Pan troglodytes, chimpanzee, modern
- (B) Australopithecus africanus, STS 5, 2.6 My
- (C) Australopithecus africanus, STS 71, 2.5 My
- (D) Homo habilis, KNM-ER 1813, 1.9 My
- (E) Homo habilis, OH24, 1.8 My
- (F) Homo rudolfensis, KNM-ER 1470, 1.8 My
- (G) Homo erectus, Dmanisi cranium D2700, 1.75 My
- (H) Homo ergaster (early H. erectus), KNM-ER 3733, 1.75 My
- (I) Homo heidelbergensis, "Rhodesia man," 300,000 - 125,000 y
- (J) Homo sapiens neanderthalensis, La Ferrassie 1, 70,000 y
- (K) Homo sapiens neanderthalensis, La Chappelle-aux-Saints, 60,000 y
- (L) Homo sapiens neanderthalensis, Le Moustier, 45,000 y
- (M) Homo sapiens sapiens, Cro-Magnon I, 30,000 y
- (N) Homo sapiens sapiens, modern
And how can we cross-check that those fossil sequences, as incredibly detailed and convincing as they are to any objective observer all by themselves, actually are evolutionary sequences and not just "apparent" ones created by a puckish "designer"? By DNA analysis and many other kinds of independent cross-checks, of course, which you would already know about if you weren't keeping yourself purposely ignorant on the subject so that you could cling to your preconceptions. For example:
Analysis of the human Alu Ye lineageMolecular and temporal characteristics of human retropseudogenes.
Serine hydroxymethyltransferase pseudogene, SHMT-ps1: a unique genetic marker of the order primates
Insertions and duplications of mtDNA in the nuclear genomes of Old World monkeys and hominoids
Fixation times of retroposons in the ribosomal DNA spacer of human and other primates
The emergence of new DNA repeats and the divergence of primates
Genetic diversity at class II DRB loci of the primate MHC
Structure and evolution of human and African ape rDNA pseudogenes
