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Posted

I see there are a few creationist posters here from time to time. So here is a very small amount of the evidence for common ancestry with the rest of the apes:

 

(1) Chromosome Banding Patterns

 

Here is Human Chromosome 2, alongside Chimp, Gorilla and Orang-Utan 2p,2q

 

hum_ape_chrom_2.gif

 

you can see there that the banding patterns are all pretty much the same. one major difference of course if that the other apes have 2 chromosomes there, whereas humans only have 1. However when we examine the human chromosome in more detail (which you can't from those diagrams) you find that in the centre of the human chromosome we have telomere like structures, which normally exist only at the ends of chromosomes. telomeres are a bit like the cellular lifetime counter, and a bit is lost on each cellular reproduction (with the exception of sex cells and cancer, which repair their telomeres) so if a telomere is '=' and a centromere is '8' (that is the bit of the chromosome containing the genes and so on) then the chimp, gorilla and orang utan 2p and q would look like ===888=== and ===888=== but the human 2 looks like ===888====888=== and you can still see this now in humans.

 

Telomeres are highly conserved sequences, which are primarily the same between all organisms in a group, for example all vertebrates have TTAGGG repeating over and over. In primates, between 300-5000 times. Ajacent to these regions are other regions of repeats called pre-telometric regions, which are highly variable, and vary significantly even within a species, but can be recognised between members of a species and closely related species.

 

In Humans, further evidence for a chromosome fusion, the order of these sequences (in the middle of the chromosome between the two centromere sections)

 

pretelomeric sequence, a telomeric sequence, an inverted telomeric sequence and an inverted pretelomeric sequence. so even these features are conserved.

 

note that only the 2p centromere functions now. the centromere of 2q, while remaining very clear that it was a functioning centromere, is no longer the point where the two chromatids join dusing cellular reproduction.

 

 

This sort of analysis is not limited to chromosome 2, but can be applied to the entire karyotype:

 

YunisFig2.GIF

 

The above image is just of humans and chimps.

 

 

 

(2) Endogenous Retroviral Sequences.

 

Retroviruses are a class of viruses that have their genetic material in the form of RNA and consist of groups such as the oncoviruses (e.g. HTLV-1) and lentiviruses (e.g. HIV). Normally DNA is transcribed into RNA before being read in order to produce proteins, however retroviruses use Reverse Transcriptase in order to take their own RNA and integrate it into the organisms own DNA. Like all genetic processes however, there is a risk of inaccuracy, and sometimes a retrovirus may become crippled by a mutation during reverse transcription, and hence may not be able to reproduce itself as a normal virus would.

 

Endogenous retroviruses may embed themselves into any cell in the body, and this includes the sex cells (gametes) as well as the normal body (or somatic) cells. If an ERV occurs in a sex cell that goes on to fertilise an egg (or be fertilised by a sperm) then the ERV will be present in every single cell of the new organism, including it's sex cells (well since it will be in one chromosome, initially it will only be in 50% of the sex cells).

 

Now one of the most important theories within evolution is that of random genetic drift, and this is an element of evolution that was only understood after the discovery of DNA. Genetic drift is a stochastic (statistical definition) process in which a particular allele (version of a gene), or bit of the DNA, will randomly increase and decrease in presence in the population, provided there is no selection pressure on that particlar allele or section of the DNA, and eventually it may become fixed within the population i.e. when it is present in all members of the population. This may happen to an ERV which became embedded within one particular individual; via random genetic drift it may become embedded in the whole breeding population. This occurs more rapidly in smaller breeding groups than large breeding groups.

 

The next step is the consideration of ancestry. If we have a group A, all of whose members have a particular ERV, we will call this ERV 'E1', and this group splits into 2 new groups, B and C, perhaps by a river forming in the middle of the group across which none of the organisms can cross, now both groups B and C will still have this ERV in all members. Now let us say that a new ERV is introduced into a member of group B and becomes fixed in group B. all members of group B will have this new ERV, which we will call 'E2'. now when we look at populations B and C, we see that B has both E1 and E2, and C has only E1. this means that E2 was introduced to the population B after B and C became separated. If B furter splits into Bi and Bii and Bii has a new ERV 'E3' fixed within its poulation, we find that Bi has E1 and E2, Bii has E1 E2 and E3 and population C still only has E1, so we can build up a tree of what order these different groups broke apart. An important point to note, is that we should never find a retrovirus shared between, for example, Bii and C alone, since the common ancestral group between Bii and C is the same common ancestral group with Bi: if an ERV becomes fixed in A, then all of its ancestors should have the ERV.

 

By examining ERVs, we can look at ancestral links between these populations. if we look at the presence of retroviruses within a population we can find when a particular group broke away from a different group due to the presence of the retroviruses within the group.

 

here is a chart of ERV distributions in the primates, and the phylogenetic tree constructed from it

 

retrovirus.gif

 

the above diagram is from the following paper:

 

Lebedev, Y. B., Belonovitch, O. S., Zybrova, N. V, Khil, P. P., Kurdyukov, S. G., Vinogradova, T. V., Hunsmann, G., and Sverdlov, E. D. (2000) "Differences in HERV-K LTR insertions in orthologous loci of humans and great apes." Gene 247: 265-277.

 

also we have

 

gkg496f3.gif

 

fig 3: Results of the 12 chimeric retrogenes insertional polymorphism study. The chimeras’ integration times were estimated according to the presence/ absence of the inserts in genomic DNAs of different primate species.

 

Note that u3-L1;Ap004289 is a polymorphism within the human species -- it integrated since the LCA of humans.

 

Ref: Buzdin A, et al. The human genome contains many types of chimeric retrogenes generated through in vivo RNA recombination. Nucleic Acids Res. 2003 Aug 1;31(15):4385-90.

 

 

A common creationist objection to the ERV concept is that of multiple insertions i.e. the idea that a virus might insert itself into the same place in different organisms and it becomes embedded in both organisms i.e. a human might be infected with E1, and this ERV becomes embedded in the human population, and a chimp might become infected with E1 and this also becomes embedded, however there are multiple problems with this hypothesis.

 

First and foremost, Of a genome that is 6 billion bases long, what are the odds that a ERV will be inserted into the same place? 1 in a 6 billion, right? Now, if there are 2 such ERVs, the odds are 1 in 6 billion times 1 in 6 billion for both being inserted into the same places by chance. If there are 3, you must multiply by another 1 in 6 billion. Now, since you have 12 such insertions in humans compared to the common ancestor, you have just passed the creationist number for it having occured by chance! By creationism's own criterion, their argument is invalid. The only creationist rebuttal to this is that there are hot spots, where the odds of a virus being inserted are slightly higher than other places, but there are still a great number of hotspots throughout the genomes, and given the above points, there is no reason why multiple infections would result in the same ERVs being inserted in the same locations with the same crippling errors and showing the same pattern of change with time. Again if there are multiple hotspots and multiple infections, there is no reason that there should not be ERVs that do not match the phylogenetic tree. again we see no deviances from expected inheritance patterns.

 

Secondly, there is no good reason as to why this would form the phylogenetic tree that it does. Even if there was a virus that was simultaneously capable of infecting every kind of primate from new world monkeys through to humans, there is no reason to think that this virus would actually infect every available primate and become fixed in every single population. we might well expect several to be missed i.e. we might see spider monkeys, bonobos, chimps and humans infected, but not gorillas or Orang Utan. we do not find these spurious distributions of ERVs.

 

Thirdly, we just do not find these sorts of retroviruses that have such a wide species affinity. and again, even if we did, there is no reason that the retroviruses would form the phylogenies that they do.

 

Fourthly, the retroviruses are crippled, but still identifiable as retroviruses. the retroviruses that we see in different species are crippled in the same way. If the retroviruses are the result of multiple infections, then there is no reason to expect the retroviruses to be crippled in the same way in different species.

 

Finally, additional alterations have been made to the ERV sequences over time. Since the ERVs themselves are not selected for or against, they themselves may be altered due to the same kind of genetic drift that caused them to be embedded within the population. we see inheritance of these changes too, that also match the phylogenetic tree of the presence of different ERVs.

 

Other Phylogenetic trees can be constructed in similar fashions by looking at ALU sequences (long sequences of repeating DNA) and transposons (kind of like internal viruses that only ever exist within the nucleus and copy themselves around the DNA)

 

(3) Transposons.

I will be brief with transposons since most of what needs to be said has already been said in the ERV section. Transposons are a form of internuclear parasite; they are sections of the genome that can copy and paste themselves around the rest of the genome. Again these transposons may become fixed within the population, and form the same sorts of phylogenetic profiles as ERVs. transposons are however completely independent from ERVs and function with a different mechanism (i.e. they do not use reverse transcriptase, they do not have viral coat proteins and they cannot cross cellular boundaries). The only possible mechanism of infection of another organism is via germ line cells - you may infect your children in other words, but nobody else. In this case there is absolutely no possibility for multiple insertions. The same phylogenetic trees can be constructed from independent analysis of transposons. It is these transposons which are responsible for much of the intergenic DNA and are also used in DNA fingerprinting, since cutting of certain chunks of DNA results in the same patterns for a given individual.

Posted

good post. The evidence never stops piling up, does it? Personally, i don't see how anyone could deny our inclusion into order Primates. You don't even need DNA comparison to see the resembalance in our behaviors and anatomy.

Posted

Absolutely magnificent!

 

Can one of the admins pin/sitcky this at the top? IMHO, it's *more* than worth it.

 

Mokele

  • 4 weeks later...
Posted

They look neat . kind of like snakes or monarch caterpillars.

 

Do the bands spread out because they are centrifuged to weight?

or do they creep apart under some sort of chemical reaction to a catalytic agent?

 

I mean what exactly is it that we are banking on here? :)

 

Ps the ERV insertion stats would be normalised if like a jigsaw puzzle piece they could only fit in one place.

 

Ps the narrowing sections on the strands, are they fusion for sure?

Posted
good post. The evidence never stops piling up, does it? Personally, i don't see how anyone could deny our inclusion into order Primates. You don't even need DNA comparison to see the resembalance in our behaviors and anatomy.

 

I’m well with you on that one, but don’t forget dolphins and sharks ( look at the tails) and spiders and insects ( count the legs ).

 

Mother nature will allow convergence to exploit a resource.

Posted
I’m well with you on that one, but don’t forget dolphins and sharks ( look at the tails) and spiders and insects ( count the legs ).

 

dolphin and shark tails are examples of convergent evolution or, analogies. In both cases, crescent shaped flippers are efficient for propulsion through the water, and were selected for this reason. These are different than the homologies shared by humans and other primates, the two being part of the same mammalian order. I know what you mean, reverse, but I was talking homology, and how that is applied with other features to strengthen the evidence of common ancestry. I don't know what you mean about spiders (or arachnids) and insects. they are both artropods, but are quite different from one another in many more ways than number of legs.

Posted
Do the bands spread out because they are centrifuged to weight?

or do they creep apart under some sort of chemical reaction to a catalytic agent?

The images are drawings of what stained chromosomes look like during cell division. Normally chromosomes are spread out thoughout the nucleus, but when a cell divides they are packed neatly by a variety of proteins. Certain dyes will bind to the chromosome giving the bands seen in the drawings. This is because they bind to specific regions of the chromosome, which depends on the sequence of the DNA and the way it is packed.

Posted
The images are drawings of what stained chromosomes look like during cell division. Normally chromosomes are spread out thoughout the nucleus, but when a cell divides they are packed neatly by a variety of proteins. Certain dyes will bind to the chromosome giving the bands seen in the drawings. This is because they bind to specific regions of the chromosome, which depends on the sequence of the DNA and the way it is packed.

 

Ok ….so we have at least two other agents acting on the chromosome.

The proteins and the dyes.

 

How can we tell what effect they have on the banding?

 

I’m just trying to figure out how untainted the final visual data is.

  • 2 weeks later...
Posted
sayo: just out of interest, when u called darth tater avatarial, was that an extremely linguistically-agile double-pun? or was it just a coincidence.

It was good, wasn't it? Nobody ever notices my puns. I'm impressed :)

Posted
Is this supposed to be an argument against creationism, or an argument against a literal interpretation of the book of Genesis?

Right, let's try this again.

 

Neither - it is ending evidence to disprove [a] generic criticism of evolution, which may be of interest to anti-evolution creationists.

Posted
Right' date=' let's try this again.

 

Neither - it is ending evidence to disprove [a'] generic criticism of evolution, which may be of interest to anti-evolution creationists.

 

OK.

 

I just thought that since the OP referred to "creationists" in the first sentence that he might have intended it as an argument against all creationists and not just the creationist who believes in a literal reading of Genisis.

Posted
I thought a pun was supposed to be a real word.

your allowed some artistic licence when making puns

It was good, wasn't it?

yup, double puns are quite hard to manufacture. kudos

 

 

just out of interest, what happened to my long post?

 

oh, and is avatarial a real word, or a non-standard stem of a real word?

Posted
OK.

 

I just thought that since the OP referred to "creationists" in the first sentence that he might have intended it as an argument against all creationists and not just the creationist who believes in a literal reading of Genisis.

 

Untimately it is evidence that those who do not think that humans and apes have a common ancestor will have a hard time dealing with. Granted there is a huge range of creationists, but in general from my experience, they think that humans were specially created and do not have a common ancestor with the other great apes.

Posted
Untimately it is evidence that those who do not think that humans and apes have a common ancestor will have a hard time dealing with. Granted there is a huge range of creationists,[/u'] but in general from my experience, they think that humans were specially created and do not have a common ancestor with the other great apes.

 

 

But it would seem that you agree that there are some who believe in creation and evolution?

Posted
I am in seminary and I believe in both, original life made by God and controled evolution by his divine means.

 

Do you believe that humans evolved from apes?

Posted

I believe humans are the highest species of apes and such are responsable to worship God for ourselves and all other animals, we evolved from a same origin.

Posted

I believe everything animal has a soul but different intelligences to understand their soul. So a dog has a soul but won't understand it but intelligent creatures such as other Great Apes and probably delfines understand to an extent, if not as much as Humans what it means "to be" and have a concept of self.

Posted

So all life is endowed with a soul as it is all part of Gods creation. But we have the intelligence to understand and appreciate that soul and thus participate in worship of God?

 

That seems a reasonable point of view.

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