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The Talk.Origins Archive: Exploring the Creation/Evolution Controversy

Editor's Note:
The Post of the Month contest for March 2002 was one of the toughest yet, with a crowded field of nominees that were all (in their own ways) excellent. Regrettably, only one post can win the voting each month, but there was definitely more than one candidate that deserved fame, or infamy, as the case may be. Rather than only choosing one and consigning the rest to relative obscurity on Google, I decided to immortalize both the winner and several runners-up on the t.o. archive. Hope no one objects.
--PotM Coordinator

The Devil Went Down to Talk.Origins

Post of the Month: March 2002

by Dave P

Subject:    About Aron-(ra) and my challenge to him...
Date:       March 28, 2002
Message-ID: 3ca3a1fa$0$

[Editor's note: Prior to this post, Dave P. had accepted an offer of a one-on-one debate with a contributor who uses the name Aron-Ra, as can be seen in the thread starting here].

Well, as I have discovered, the term Ra is the name given to the "sun god" that Aron is worshipping. According to my christian background and relationship with the God of the bible, Aron is getting his inspiration from the psychopath known in the bible, as satan. So, therefore, by attempting to show Aron his flaws and deception, I would be basically engaging in a debate with the devil himself and I refuse to make conversation with the devil, so my challenge to Aron (who is being inspired by satan), is off.

[Return to the 2002 Posts of the Month]

Monkeys' Uncles

Post of the Month Runner-Up: March 2002

by Floyd

Subject:    Re: A Question about Human Evolution.
Date:       March 14, 2002
Message-ID: (Freedom Warrior) wrote in message news:<>...
> Greetings everyone. If you don't mind, I would like to ask any of
> you that are experts on biological evolution this question.
> I am aware of the creationist lies about human evolution stating
> that man came from monkeys, which is not true of course. Man did not
> evolve from monkeys and apes, we came from a common ancestor along with
> primates (feel free to correct me if I am wrong).
> The question that I wanted to ask is, what is the name of that
> "common ancestor" where humans and primates evolve from?
> Thanks!

You've received some good responses (as well as some predictable creationist drivel) and I just wanted to add my two scents ('cause primatologists think us paleoanthropologists stink ;-) In answer to your question, it depends on which particular MRCA you're looking for.

Phenacolemur jepseni was a Plesiadapiforme that lived about 60 MYA, and some researchers consider the Plesiadapiformes to be the common ancestor of all the primates. It's difficult to know for certain which (if indeed any) of the Plesiadapiforme species was "the" ancestor, but I personally feel confidently that if it was not P. jepseni, it was a close relative. The reason for the difficulty in identifying the species is that the only trait that all primates share, but that is not shared with other mammals, is the "petrosal bulla," part of the skull that surrounds the inner ear. In some non-primates, the bullae fuse to the petrosal in adulthood, so in order to tell if a questionable species was a primate, juveniles have to be found. Juveniles don't fossilise as easily as adults, and they are much less frequently recovered, because of their size (c.f. Behrensmeyer 1978, Butler and Chatters 1994, e.g.). Still, P. jepseni juveniles did posess the fused petrosal bulla, suggesting that they were, or were closely related to, the ancestor of all living primates.

The arthropoids split from the prosimians some time between 40 and 45 MYA and by the early Oligocene, a few species that could be recognized as members of our own suborder, Anthropoidea, could be found. Among the most well studied of these early "monkey-like" Anthropoids are Apidium and Aegyptopithecus. Apidium was about the size of a big rat, maybe three pounds at most, and in my opinion, the larger (10-20 pound) Aegyptopithecus was the more likely of the two to be ancestral to the living "Old World" primates. The Oligocene is not particularly rich in primate fossils though, and it's difficult to make any certain claims.

Remember that at this time, North America (the "original homeland" of the primates) was still connected to Europe. As the northern "supercontinent" (which I've heard called "Laurentia") split up, the ancestors of the New World monkeys were separated from the ancestors of all of the Old World primates, both monkeys and apes.

By the early Miocene (23-16MYA), the apes split from the monkeys. There are several well-known Miocene apes, whih paradoxically makes it harder, rather than easier, to determine which of them is the most likely [monkey+ape] MRCA. This is especially true of the middle Miocene (18-11 MYA or so). Andrew Hill and colleagues (as mentioned in Scientific American 30 August 1999) have presented the genus Equatorius (formerly Kenyapithecus africanus) which is as good a candidate for the ape/Old World monkey split as I've seen. (See Of course again, there is no way to know for certain which species of this genus, as opposed to a closely related but currently undiscovered one, is "the" ancestor, or even if that species lived immediately before or shortly after the split. Nevertheless, it was around that time, and if it wasn't E. africanus, it was probably a close relative.

The late Miocene apes are a complete morass right now; there've been dozens of proposed relationships, none of which has garnered wide, much less general acceptance. Again, the reason for this is an "embarassment of riches." We simply have so much stuff from this period that we're having trouble organising it all. Most paleoanthropologists and paleoprimatologists agree that Ramapithecus is really Sivapithecus, and Gigantopithecus is a sister group. One of these (probably Sivapith..) is ancestral to the modern orang-utans. Dryopithecus and Ouranopithecus are both candidates for ancestors of Hominoids. It was around this time (maybe 10-12 MYA) that the gorilla line split from the human+chimp group, so this is where we should look for that MRCA. One interesting possibility is Motopithecus, but this genus is known from pretty fragmentary evidence so far, and the teeth look a bit more gorilla-like than human like. Besides, it's a "mere" 8 million years old, so it's probably on the gorilla side of the split, or a closely related sister group.

Pliocene apes are less well known, presumably because the climate of Africa and south Asia (where they lived at the time) was less suitable to fossilisation than earlier. Climate became much warmer and wetter, which caused forests to spread, and as others have mentioned, forests are generally unsuitable for fossil formation ("diagenesis"). The soil in lush, wet forests tends to be much more acidic, which causes rapid bone decomposition (although in some anaerobic conditions, highly acidic deposits can preserve "soft" tissue, and I always hope that we'll some day find some of the "squishy parts" of our Pliocene ancestors; wouldn't that be great?) It's too bad that we don't know the Pliocene apes better, because it's around this time that our ancestors split from the ancestors of the chimps. Others have mentioned Ardipithecus ramidus, and Orrorin tugenensis also looks like a possibility. Tragically, we don't yet have anything that might be the MRCA of Pan paniscus and P. troglodytes, but we keep finding new stuff on "our" side of that split, pretty much every year. Much of it is detailed in the fossil hominid FAQ at

Hope that was helpful.

[Return to the 2002 Posts of the Month]

Mechanisms of Gene Transfer in Bacteria

Post of the Month Honorable Mention: March 2002

by David Tamang

Subject:    Re: Am I missing the Point of 'Science'?
Date:       March 20, 2002
Message-ID: sY5m8.174564$

"Victor Eijkhout" <> wrote in message
> David Tamang <> wrote:
> > Actually, resistance to antibiotics comes about by a fundamental change in
> > the bacteria's genome through external mechanisms such as viral DNA
> > incorporation or plasmid transfer.
> And can you convincingly make the case that this is not a
> white-vs-black-moth phenom, the resistant bacteria already existing, but
> now suddenly getting selected since the rest is killed off by
> antibiotics?
> V.

Yes, actually. First, because you obviously don't understand plasmid and other mechanisms of genetic transfer in bacteria, I suggest you do some background reading. You will find a college level textbook to have the necessary information on plasmid transfer. Information concerning viral incorporation of new traits will have to be found in a new, graduate level text as useful material in this context is only 5-7 years old or so. I suggest Molecular Cell Biology, 4th Ed. by Lodish, Berk, et al., published by Freeman Press. For one of the newest methods of genetic modification in bacteria, pathogenicity islands, you have to go to professional journals as the material is too recent to have been published in any texts, I believe. I suggest the following articles:

1: Ehrbar K, Mirold S, Friebel A, Stender S, Hardt WD.
Characterization of effector proteins translocated via the SPI1 type III secretion system of Salmonella typhimurium.
Int J Med Microbiol. 2002 Feb;291(6-7):479-85.
PMID: 11890547 [PubMed - in process]

2: Fischer W, Puls J, Buhrdorf R, Gebert B, Odenbreit S, Haas R.
Systematic mutagenesis of the Helicobacter pylori cag pathogenicity island: essential genes for CagA translocation in host cells and induction of interleukin-8.
Mol Microbiol. 2001 Dec;42(5):1337-48.
PMID: 11886563 [PubMed - in process]

3: Yarwood JM, McCormick JK, Paustian ML, Orwin PM, Kapur V, Schlievert PM.
Characterization and expression analysis of Staphylococcus aureus pathogenicity island 3: implications for the evolution of staphylococcal pathogenicity islands.
J Biol Chem. 2002 Jan 30 [epub ahead of print]
PMID: 11821418 [PubMed - as supplied by publisher]

I'm not sure if these are accessible on the internet for free or not. But you can get them if you go to your local university.

Now, to answer your question. There are two fundamental differences between the moth wing business and genetic resistance in bacteria. Concerning moth phenotypes, the genetic expression is based on Mendelian principles, that is incomplete dominance, multiple alleles, interacting recessive/dominant traits, etc. This provides for horizontal evolution, but not vertical evolution, and I think this is the point you're getting at. The key aspect of Mendelian genetics, however, is that the genes necessary to express any of the possible phenotypes are present in all of the organisms of a given species. It's merely a question of selective pressures determining the frequency of which alleles get expressed.

In regard to bacterial resistance to antibiotics, the genetic material necessary to code for proteins facilitating the removal of antibiotics from the microbe is not encoded in the DNA of the bacterium. In fact, in colonies of non-resistant bacteria, there is no genetic modification to produce strains resistant and all will die out. However, if you introduce plasmids containing resistant genes to a colony of bacteria, they will incorporate this genetic material into their own genome and produce the proteins that prevent antibiotic effectiveness.

This incorporation of genetic material operates outside Mendelian laws and in theory can result in vertical evolution of single celled organisms. In fact, it's one of the strongest arguments for observation of macro evolution on a micro time scale.

Exactly how these new strands of DNA support genetic modification with regard to enhancing bacteria survival characteristics is not known at this time. What we do know is that the sequences are not present in the genome before incorporation. Fully sequenced genomes in E. coli, a model organism for these types of studies, have shown the absence of new genes found after assimilation of genetic material from external sources.

It has been suggested that interaction between viruses and bacteria is more involved than we originally thought. Researchers propose that viruses, after hijacking the biomechanical machinery in a cell, will modify the genetic code to include these advantageous traits. It's assumed the benefit of this is the virus gets to hang around longer in the bacteria and make more copies of itself while the bacteria gets genetic variation that can be quite advantageous. There is no proposed mechanism for this event that I am aware of.

The Pathogenicity Islands have shown to modify characteristics of organism so radically, they can change benign E. coli normally found in intestinal flora into a toxin-producing pathogen resulting in acute gastritis. The complete mechanism for this is not known either, but studies have shown entire genetic sequences between the P.island have translocated. This is a radical change in the genome. Apparently, the enzymes necessary to do the splicing are encoded by the islands themselves and read the original sequences. A paper was published in November of last year showing that this phenomena occurs in V. cholerae as well.

5: Dalsgaard A, Serichantalergs O, Forslund A, Lin W, Mekalanos J, Mintz E, Shimada T, Wells JG.
Clinical and environmental isolates of Vibrio cholerae serogroup O141 carry the CTX phage and the genes encoding the toxin-coregulated pili.
J Clin Microbiol. 2001 Nov;39(11):4086-92.
PMID: 11682534 [PubMed - indexed for MEDLINE]

This is a quick overview of a couple common ways bacteria demonstrate potential for vertical evolutionary change. If you peruse the reading I suggested, you should be able to find more complete descriptions of what's going on the molecular/chemical level.

Whew, I hope this was convincing enough for you.

[Return to the 2002 Posts of the Month]

What's the Urgency?

Post of the Month Honorable Mention: March 2002

by Mike Dunford

Subject:    What *is* the urgency, anyway? (was: Re: Dembski and Weasels)
Date:       March 3, 2002
Message-ID: 3c81d650.9113664@news-server

On 2 Mar 2002 19:34:21 -0500, (Mike Goodrich) wrote:
> (Ron Okimoto) wrote in message news:<>...


>> So mg, where is your analysis of my shallow commentary. I gave a
>> specific example that showed that Dembski was full of baloney. Apply
>> his filter to the antibody system and what do you get? You seem to be
>> the self appointed expert and since Dembski isn't around to enlighten
>> us why don't you show us how the filter works for the antibody system.
>> Why hasn't Dembski done it? If you were Dembski wouldn't you want to
>> apply your ideas to a real biological system?
>So what's the urgency, Ron?
>Basic, groundbreaking research and conceptual development
>can't be required to satisfy the tyranny of the urgent.
>All things in good time.

This actually brings up an important question: with the entire body of ID work at a very primitive state, as even its proponents acknowledge, why is there such a massive rush to cram ID into the schools?

Even if we accept at face value the claims made by the Design camp, that ID represents a legitimate, promising avenue of scientific research, the conclusion that this avenue is at present largely unexplored is unavoidable. In fact, many of the key players in the ID community admit that their speculations are not yet well supported by empirical data, and that more research is needed.

One good example of this is given by Dembski in his introduction to Mere Creation: Science, Faith, and Intelligent Design (1998):

"Intelligent design is a fledgling science. Even so, intelligent design is a fledgling of enormous promise. Many books and articles are in the pipeline. I predict that in the next five years intelligent design will be sufficiently developed to deserve funding from the National Science Foundation." (p29)

So, even according to one of the driving forces behind the movement, ID is still likely over a year away from being ready for initial public funding. Why, then, is there a massive rush to teach this 'fledgling' in the public schools right now?

If the proponents of the design speculation actually intended to pursue their ideas as purely scientific concepts, one would expect them to focus on doing the necessary research to advance their hypothesis. In fact, such primary research has been at best uncommon, and the proponents have instead concentrated their time on politically advancing their cause as an opponent to 'Darwinism'.

This is not the behavior expected of scientists. Others have had their ideas mocked and have later been vindicated. Proponents of sea-floor spreading, for example, were not initially taken seriously. Rather than interrupt their research to try to convince school boards to teach their ideas, they continued to amass and publish convincing evidence. Once their theory was well established, it began to be included in textbooks and taught in classes. That is the way science and education have always worked -- high school texts typically lag behind undergraduate texts, which also tend to be several years behind the cutting edge. This is a safety factor which is built in to education -- much of the research which initially appears to be highly promising later turns out to be a dud. Having a lag between this material and the basic, introductory-level courses keeps beginning students from being confused by rapidly changing materials.

The behavior of the ID movement is inconsistent with the legitimate advancement of scientific research. It is, however, what would be expected from a group designed to provide support to opponents of evolution. The vast bulk of the material published by IDers focuses on the supposed weaknesses and inconsistencies in their opponent's theory. Very little work has been done which provides direct support for their position, and less of that has been supported by actual original research. If the ID movement is a smokescreen, we should expect to see more of the same. Certainly, we should not expect to see any original research in the biological sciences performed by IDers which has the slightest potential to falsify their position. As a political movement, they have little to gain and everything to lose by taking such risks.

--Mike Dunford

[Return to the 2002 Posts of the Month]

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