Do Chimps and Humans Share a Common Ancestor?

mark kennedy · #1 3rd July 2007, 07:13 PM

I am a young earth creationist with an avid interest in the life sciences from a fundamentalist point of view. I am opposed to evolution as natural history, specifically, I consider the human/chimp common ancestor to be a modern myth.

This is an open invitation to anyone interested in debating the topic formally. I am flexible of the source material and the specifics of the topic. However, I am unbending with regards to the forum rules of debate. You would be free to post whatever you see fit, invite anyone you like to participate and I am not thin skinned. I won't wear my heart on my sleeve if someone wants to be harsh or critical. Post length restrictions as defined in the formal debate forum rules are nonnegotiable. Double posts will result in a forfeit which has to be agreed to in advance of the opening statements.

I have a special interest in the life sciences, paleontology and the Bible as history. If you are interested feel free to post whatever questions, concerns or proposals you wish to have addressed. If I do not respond in a timely manner in could mean I am not monitoring the thread. In that event I would appreciate a PM to let me know that you have expressed an interest.

This area is running over with evolutionists in the common forum, surely there is one with the courage of their convictions to take this up.

Have a nice day

Mark

R3quiem · #2 6th July 2007, 08:28 PM

Ok. You seem like you are impossible to convince otherwise, but I'll at least show you the way I look at it.

Genetics
Well the first argument that is usually used is genetics. When compared, chimp DNA is very similar to human DNA. All apes are closely related by their DNA. Supposedly, the genetic different between rats and mice is much larger than the genetic difference between humans and chimps.

Skeleton Comparison
Also, look at a human skeleton compared to a chimp skeleton, orangutan skeleton, and a gorilla skeleton. The most obvious difference is that we stand upright. When one of those apes' skeletons are stood upright, it looks eerily similar to our own- just with longer arms and slightly different proportions.

Ancient Humans
I guess the most convining argument for ape-human evolution for me is that found in the skeletons of ancient humans. If you look at dozens of ancient skulls, that spanned over millions of years (although you won't believe that, because you believe in a young earth), they slowly transform from ape-looking to human-looking.

For example, homo erectus was around for a while. He stood upright, but had very ape-looking features, such as a larger jaw and a smaller brain cavity. Different human species broke off from him, including neanderthals and eventually homo sapiens (us). Neadnerthals and sapiens have remains that are found in the same areas and are believed to be around at the same time. It is believed that Neanderthals didn't fully go extinct until 12,000 to 30,000 years ago, as they were out-paced by the sapiens.

If you don't believe in ape-human evolution, what is your view on all of the many, many remains of these ancient humanoids?

mark kennedy · #3 7th July 2007, 07:22 PM

Originally Posted by R3quiem

Ok. You seem like you are impossible to convince otherwise, but I'll at least show you the way I look at it.

Happy to hear you out.

Genetics
Well the first argument that is usually used is genetics. When compared, chimp DNA is very similar to human DNA. All apes are closely related by their DNA. Supposedly, the genetic different between rats and mice is much larger than the genetic difference between humans and chimps.

That's just fine, I have no problem with that approach. All I ask is the the inverse logic be allowed, when the differences cannot be accounted for it opens up special creation as at least a possibility. They are not really as close as they are telling you and what is more the molecular mechanism for the evolution of the human brain is a complete mystery to the researchers. It does not automatically mean that God did it, it just means that the a priori assumption the God didn't do it is unfair and ill founded.

Skeleton Comparison
Also, look at a human skeleton compared to a chimp skeleton, orangutan skeleton, and a gorilla skeleton. The most obvious difference is that we stand upright. When one of those apes' skeletons are stood upright, it looks eerily similar to our own- just with longer arms and slightly different proportions.

How many chimpanzee ancestors do we have from about 2 million years ago? The answer is none, every time an ape fossil is dug up it is automatically considered one of our ancestors. This is the same desperate bias that made the Piltdown hoax so appealing for half a century and it's still distorting the evidence.

Ancient Humans
I guess the most convining argument for ape-human evolution for me is that found in the skeletons of ancient humans. If you look at dozens of ancient skulls, that spanned over millions of years (although you won't believe that, because you believe in a young earth), they slowly transform from ape-looking to human-looking.

Homo habilis is an ape with a cranial capacity and other anatomical features that are far more ape then human. The Homo erectus explodes on the scene with a cranial capacity twice what it is for African and Asian apes. All other physical characteristics are absolutly human except for a couple of small brained individuals that have cranial capacities well within human limits.

Homo erectus was human, Homo habilis was not. Notice, there is nothing in the middle.

For example, homo erectus was around for a while. He stood upright, but had very ape-looking features, such as a larger jaw and a smaller brain cavity. Different human species broke off from him, including neanderthals and eventually homo sapiens (us). Neadnerthals and sapiens have remains that are found in the same areas and are believed to be around at the same time. It is believed that Neanderthals didn't fully go extinct until 12,000 to 30,000 years ago, as they were out-paced by the sapiens.

Neanderthals actually had a cranial capacity 10% larger then our own. Just like Homo habilis had a cranial capacity that was 10% larger then the chimpanzee. Neanderthals burst on the scene some 130,000 years ago with a cranial capacity of 1600cc. That means that in just over a million years the cranial capacity had tripled. That would all be well and good if they had a clue what the molecular mechanism was for a large scale adaptive evolutionary trend like that was.

If you don't believe in ape-human evolution, what is your view on all of the many, many remains of these ancient humanoids?

Some are human, many others are the missing links between the original chimpanzees and modern ones. If you go far enough back in the mythical natural history gorillas have their ancestors represented.

Thanks for the exchange, if you interested in the debate I'm open to your proposal. Otherwise I'll see you on the boards.

mark kennedy · #4 13th July 2007, 07:08 PM

This is the bibliography I promised. Once I have yours you can feel free to start the Opening Post or just let me know you are ready for me to. If someone else barges into the debate I would ask that they be ignored. I intend to report any intrusions but I don't know that the moderators will care.

My thesis is pretty simple really, the deleterious affects of mutations prevent evolution on the scale required for humans to evolve from apes. No need for a retort right now, just post the bibliography and we can get started any time you are ready.

Here we present a draft genome sequence of the common chimpanzee (Pan troglodytes). Through comparison with the human genome, we have generated a largely complete catalogue of the genetic differences that have accumulated since the human and chimpanzee species diverged from our common ancestor, constituting approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements. We use this catalogue to explore the magnitude and regional variation of mutational forces shaping these two genomes, and the strength of positive and negative selection acting on their genes. In particular, we find that the patterns of evolution in human and chimpanzee protein-coding genes are highly correlated and dominated by the fixation of neutral and slightly deleterious alleles. We also use the chimpanzee genome as an outgroup to investigate human population genetics and identify signatures of selective sweeps in recent human evolution.

Initial sequence of the chimpanzee genome and comparison with the human genome

Human–chimpanzee comparative genome research is essential for narrowing down genetic changes involved in the acquisition of unique human features, such as highly developed cognitive functions, bipedalism or the use of complex language. Here, we report the high-quality DNA sequence of 33.3 megabases of chimpanzee chromosome 22. By comparing the whole sequence with the human counterpart, chromosome 21, we found that 1.44% of the chromosome consists of single-base substitutions in addition to nearly 68,000 insertions or deletions. These differences are sufficient to generate changes in most of the proteins. Indeed, 83% of the 231 coding sequences, including functionally important genes, show differences at the amino acid sequence level. Furthermore, we demonstrate different expansion of particular subfamilies of retrotransposons between the lineages, suggesting different impacts of retrotranspositions on human and chimpanzee evolution. The genomic changes after speciation and their biological consequences seem more complex than originally hypothesized.

DNA sequence and comparative analysis of chimpanzee chromosome 22

Evolution of the Human ASPM Gene, a Major Determinant of Brain Size
Jianzhi Zhang, Genetics, December 2003

The size of human brain tripled over a period of ~2 million years (MY) that ended 0.2–0.4 MY ago. This evolutionary expansion is believed to be important to the emergence of human language and other high-order cognitive functions, yet its genetic basis remains unknown. An evolutionary analysis of genes controlling brain development may shed light on it. ASPM (abnormal spindle-like microcephaly associated) is one of such genes, as nonsense mutations lead to primary microcephaly, a human disease characterized by a 70% reduction in brain size. Here I provide evidence suggesting that human ASPM went through an episode of accelerated sequence evolution by positive Darwinian selection after the split of humans and chimpanzees but before the separation of modern non-Africans from Africans. Because positive selection acts on a gene only when the gene function is altered and the organismal fitness is increased, my results suggest that adaptive functional modifications occurred in human ASPM and that it may be a major genetic component underlying the evolution of the human brain.

AMONG mammals, humans have an exceptionally big brain relative to their body size. For example, in comparison with chimpanzees, the brain weight of humans is 250% greater while the body is only 20% heavier (MCHENRY 1994 Down). The dramatic evolutionary expansion of the human brain started from an average brain weight of 400–450 g ~2–2.5 million years (MY) ago and ended with a weight of ~1350–1450 g ~0.2–0.4 MY ago (MCHENRY 1994 Down; WOOD and COLLARD 1999 Down). This process represents one of the most rapid morphological changes in evolution. It is generally believed that the brain expansion set the stage for the emergence of human language and other high-order cognitive functions and that it was caused by adaptive selection (DECAN 1992 Down), yet the genetic basis of the expansion remains elusive. A study of human mutations that result in unusually small brains may help identify the genetic modifications that contributed to the human brain expansion. In this regard, primary microcephaly (small head) is of particular interest (MOCHIDA and WALSH 2001 Down; BOND et al. 2002 Down; KUMAR et al. 2002 Down). Microcephaly is an autosomal recessive genetic disease with an incidence of 4–40 per million live births in western countries (MOCHIDA and WALSH 2001 Down; KUMAR et al. 2002 Down). It is defined as a head circumference >3 standard deviations below the population age-related mean, but with no associated malfunctions other than mild-to-moderate mental retardation (MOCHIDA and WALSH 2001 Down; KUMAR et al. 2002 Down). The reduction in head circumference correlates with a markedly reduced brain size. Microcephaly is genetically heterogeneous, associated with mutations in at least five loci (MOCHIDA and WALSH 2001 Down; KUMAR et al. 2002 Down), one of which was recently identified and named ASPM (abnormal spindle-like microcephaly associated; BOND et al. 2002 Down). Four different homozygous mutations in ASPM introducing premature stop codons were found to cosegregate with the disease in four respective families, while none of these mutations were found in 200 normal human chromosomes (BOND et al. 2002 Down). Because the brain size of a typical microcephaly patient (430 g; MOCHIDA and WALSH 2001 Down; KUMAR et al. 2002 Down) is comparable with those of early hominids such as the 2.3- to 3.0-MY-old Australopithecus africanus (420 g; MCHENRY 1994 Down; WOOD and COLLARD 1999 Down), I hypothesize that ASPM may be one of the genetic components underlying the human brain expansion. Signatures of accelerated evolution of ASPM under positive selection during human origins would strongly support my hypothesis, because the action of positive selection indicates a modification in gene function resulting in elevated organismal fitness (ZHANG et al. 2002 Down). Below I provide population genetic and molecular evolutionary evidence for the operation of such adaptive selection on ASPM.
-------------------------------------------------
The Evolution of Mammalian Gene Families (Jeffery P. Demuth, Tijl De Bie, Jason E. Stajich, Nello Cristianini, and Matthew W. Hahn PLoS ONE.December 20, 2006)

http://www.pubmedcentral.nih.gov/art...?artid=1762380

Abstract
Gene families are groups of homologous genes that are likely to have highly similar functions. Differences in family size due to lineage-specific gene duplication and gene loss may provide clues to the evolutionary forces that have shaped mammalian genomes. Here we analyze the gene families contained within the whole genomes of human, chimpanzee, mouse, rat, and dog. In total we find that more than half of the 9,990 families present in the mammalian common ancestor have either expanded or contracted along at least one lineage. Additionally, we find that a large number of families are completely lost from one or more mammalian genomes, and a similar number of gene families have arisen subsequent to the mammalian common ancestor. Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives.

--------------------------------------------------

Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000)

Abstract
Many previous estimates of the mutation rate in humans have relied on screens of visible mutants. We investigated the rate and pattern of mutations at the nucleotide level by comparing pseudogenes in humans and chimpanzees to (i) provide an estimate of the average mutation rate per nucleotide, (ii) assess heterogeneity of mutation rate at different sites and for different types of mutations, (iii) test the hypothesis that the X chromosome has a lower mutation rate than autosomes, and (iv) estimate the deleterious mutation rate. Eighteen processed pseudogenes were sequenced, including 12 on autosomes and 6 on the X chromosome. The average mutation rate was estimated to be ~2.5 x 10-8 mutations per nucleotide site or 175 mutations per diploid genome per generation. Rates of mutation for both transitions and transversions at CpG dinucleotides are one order of magnitude higher than mutation rates at other sites. Single nucleotide substitutions are 10 times more frequent than length mutations. Comparison of rates of evolution for X-linked and autosomal pseudogenes suggests that the male mutation rate is 4 times the female mutation rate, but provides no evidence for a reduction in mutation rate that is specific to the X chromosome. Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common.
MUTATION is the ultimate source of genetic variation; it is both the substrate for evolution and the cause of genetic disease. Most previous estimates of the human mutation rate have utilized one of three approaches. Two of these approaches rely on phenotypic differences associated with diseases and the third approach relies on direct comparison of DNA sequences without function. These phenotypic and molecular methods are fundamentally different and rely on different assumptions. The first approach, pioneered by HALDANE 1932 , HALDANE 1935 , assumes diseases are in mutation-selection balance.
---------------------------------------------------
Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes

4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8

Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
-----------------------------------------------------

Table 4. Estimates of mutation rate for different sites and different classes of mutation

Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8

Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.
---------------------------------------------------------

Nielsen R, Bustamante C, Clark AG, Glanowski S, Sackton TB, et al. A scan for positively selected genes in the genomes of humans and chimpanzees. PLoS Biology. 2005

Carroll SB. Evolution at two levels: on genes and form. PLoS Biology. 2005

Wang X, Grus WE, Zhang J. Gene losses during human origins. PLoS Biology. 2006

May the truth prevail,
Mark

Jet Black · #5 17th July 2007, 08:06 AM

if and only if mark doesn't use the same tired old arguments that he always uses, that have been falsified over and over again.

Loudmouth · #6 18th July 2007, 04:47 PM

I will focus on ERV's as evidence of common ancestry. I will be using the sources below:

Herpes integration
link

integration sites HIV and aslv
http://www.pubmedcentral.nih.gov/art...medid=16140779

integration sites for HIV, ASLV, and MLV
http://www.ncbi.nlm.nih.gov/sites/en...ubmed_RVDocSum

Sequence and placement comparison of ERV's shared by humans, chimps, gorillas, bonobos, and african green monkey
http://www.pubmedcentral.nih.gov/art...medid=10468595

Shared ERV in humans, chimps, and orangutans. There is a great picture of a Southern blot on pg. 1639.
http://vir.sgmjournals.org/cgi/reprint/77/8/1631

Good secondary article by GR Morton
http://home.entouch.net/dmd/hegene.htm

The talkorigins section on ERV's
http://www.talkorigins.org/faqs/comd...l#retroviruses

mark kennedy · #7 18th July 2007, 07:32 PM

Excellent! Thanks for posting the primary source material links you will be using. While I am looking it over just give some thought to any parameters or conditions in the formal debate.

Feel free to open up the discussion of the rules and conditions at your discretion. My only concern is post length and number. If need be I am open to more rounds by mutual consent but the length limits of CF must be the limit of your response. The opening post and closing remarks can be anything you like since I don't anticipate a lot of off topic tangents.

It has been my experience that expositions or an opponents post takes up way too much room. I would suggest focusing on the details of the scientific literature whenever possible.

I'm looking forward to the formal LM and I'll monitor the thread for any further posts.

Loudmouth · #8 20th July 2007, 12:11 PM

I propose that the debate be broken up into 5 posts as follows

Post 1: Opening statements, argument
Post 2: Discuss opponents Post 1
Post 3: Discuss opponents Post 2
Post 4: Discuss problems with opponents argument and opponents refutation of your own argument. This post will focus on specific issues.
Post 5: Closing arguments

I agree with mark that posts should be limited to the CF limit imposed on each post. I would prefer if rebuttals and refutations were not a sentence by sentence quote fest like it often is in informal threads. It is much better to get a feel for your opponents argument and sum it up as accurate but succinctly as possible.

Does this sound good, mark kennedy?

PS: I will also be asking sfs for some help if that is ok. I haven't asked for his help yet, but since he is an author on the chimp genome paper I can't help but run some ideas by him.

mark kennedy · #9 20th July 2007, 06:17 PM

Originally Posted by Loudmouth

I propose that the debate be broken up into 5 posts as follows

Post 1: Opening statements, argument
Post 2: Discuss opponents Post 1
Post 3: Discuss opponents Post 2
Post 4: Discuss problems with opponents argument and opponents refutation of your own argument. This post will focus on specific issues.
Post 5: Closing arguments

I agree with mark that posts should be limited to the CF limit imposed on each post. I would prefer if rebuttals and refutations were not a sentence by sentence quote fest like it often is in informal threads. It is much better to get a feel for your opponents argument and sum it up as accurate but succinctly as possible.

Does this sound good, mark kennedy?

PS: I will also be asking sfs for some help if that is ok. I haven't asked for his help yet, but since he is an author on the chimp genome paper I can't help but run some ideas by him.

Sounds great, sfs is welcome to participate at his discretion as long as post length is not exceeded. The number of rounds not counting OP and closing remarks would appear to be three. It could be expanded if you like but that is entirely up to you as far as I'm concerned. One of us should start a thread in the common forum so anyone interested in commenting on the debate can be directed there.

At this point I see no problems. Since I am not entirely sure where you are taking me with this exchange over the ERVs I'll let you make the first OP. My interests are adaptive evolution and the molecular mechanisms that produce them. This debate will be focused on evolution after all and adaptations are the prize.

I appreciate your willingness to engage me on this issue and look forward to the exchange.

May the truth prevail,
Mark

[edited to add: Just one more thing, I am waiving the time constraints from my end. You have taken some time between posts so I expect your busy and I'm in no big rush myself. If on the other hand you think a response in a timely manner is essential you have only to express your concern.

Loudmouth · #10 20th July 2007, 06:42 PM

Originally Posted by mark kennedy

My interests are adaptive evolution and the molecular mechanisms that produce them. This debate will be focused on evolution after all and adaptations are the prize.

Then you need to look at the title of this thread. The focus of the debate is whether or not humans and chimps share a common ancestor.

I am going to be gone this weekend and intend to have a post ready either monday or tuesday. I, too, am looking forward to this debate.