scigirl

When did I do this?
Thorougly and completely? (Scigirl busts a gut laughing). As usual, the creationist failed to take into account any other type of mutation, such as gene duplications, transversions, and jumping genes.
No it does not, see above.

I started a thread for you about the evidence that humans and chimps share a common ancestor: it's called "Question for JFoard"

scigirl

Edited to add link to the "question" thread:
<a href="http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001134" target="_blank">http://iidb.org/cgi-bin/ultimatebb.cgi?ubb=get_topic&f=58&t=001134</a>

[ July 23, 2002: Message edited by: scigirl ]</p>

scigirl

I just found a great site that explains some of the "other" types of genetic alterations that can act as a source for evolution:

<a href="http://www.catalase.com/evogenedup.htm" target="_blank">http://www.catalase.com/evogenedup.htm</a>

NOTE: those calculations you read on creationist sites never take these into account. We really have no clue to even quantify some of these phenomenon, so if someone told you that "evolution is improbable according to my calculations," they are wrong.

scigirl

l-bow

Why don't these creationists get it? Speciation is the creation of a new specie from an older specie. So naturally a fruit fly will still be a fruit fly. What they of course want is something else, let's call it "kind-ation", the creation of a new "kind" from a older "kind".

I wonder if the creationist leaders are misleading their followers deliberately on this point?

Jack the Bodiless

No, YOU have missed the point. Every single one of us AGREES that the peppered moth is not an example of SPECIATION, and it has never been presented as such by any "evolutionist". It is, however, an example of NATURAL SELECTION, one of the two key principles of EVOLUTION (the other being mutation).

This is a strawman argument.

Again, YOU are missing the point. There are no "kinds". When speciation occurs, and two non-interbreeding populations are established, divergent evolution is inevitable from then on. And we have an abundance of cladistics, DNA and fossil evidence to show that this has indeed happened.

For instance, we know that dogs and bears are of the same "kind". Go back further, and the bear/dog kind also includes felines. And so on.

As for the article:
Mutations which add information to a genome are well-known. So we have now established that Fred Williams is a liar.
Harmful mutations do not achieve "fixation". A random neutral mutation can either spread or shrink within a population, by sheer chance (genetic drift). Even a small bias in favor of shrinkage (the harmfulness of the mutation) will cause elimination over time. This is entirely independent of the rate at which new harmful mutations are being introduced. Williams is failing to allow for the fact that all these harmful mutations are being reduced in parallel throughout the population. His argument would work only if all harmful mutations were of the same type.

For instance, let's assume that a thousand copies of a mutation we'll call "BAD" are coming into a population in each generation, and that it takes a century for a thousand copies of BAD to be eliminated entirely even if it was no longer being generated. In this scenario, it's easy to see that BAD will overwhelm the population. However, if only a dozen copies of BAD are being generated (along with a dozen copies of BAD2, a dozen of BAD3, and so on), and a thousand existing copies of EACH variant of BAD can still be eliminated in a century... there is no problem!

pseudobug

Oh, Mr. Foard, so sorry you and Dr. Haldane do not have the imagination or knowledge to understand just how we might differ from our dung throwing cousin. Humans and chimps are thought to have a common ancestor (although in your case I think you may have been derived from a chimp).

No matter, that isn't what is important.

First, 1700 heritable mutations is quite a lot, particularly if they led to phenotypic differences. COnsider that a typical biochemical pathway may have 10 steps--each encoded by a different gene. In that case, the result could be alterations in 160 different pathways if the result of each mutation affected only one particular pathway (highly unlikely as some changes, particularly regulatory gene, can effect multiple pathways).

Another thing that you and Haldane do not consider are differences in genes controlling development. Sadly for you, Haldane had an excuse--hox genes were not discovered until ~30 years after he enunciated his dilemma. But again, I digress. Imagine that there is a single crucial hox gene or a single crucial target of hox gene regulation that is expressed in a temporally or spatially different manner in humans that allows our brains to develop in such a manner as to acquire/develop speech. Would that not have a profound impact on differences in the species? Keep in mind the fact that these developmental genes also have a profound impact on morphological differences as well and perhaps you can imagine why the "evolutionists" are so different from "dung throwers" such as yourself.

[ July 24, 2002: Message edited by: pseudobug ]</p>

KC

JFoard apparently did not read my post very well.

A):His example about mutation rates misses an essential point:I was talking about divergence which is the accumulation of variation between populations. This includes neutral mutation, which is a significant chunk of mutation in general. Natural slection will eliminate the deleteiuous mutations, but it will favor beneficial, and it wont effect neutral variation. THat is why I included the stochastic processes like drift, which will affect gene frequencies on both beneficial and neutral mutations. It is the accumulated genetic DIFFERENCES (regardless of beneficial or neutral in regards to fitness) that eventually result in the post-zygotic reproductive isolation and speciation. So no, JFOARD, it hasn't been 'dealt with', and you can't 'throw it out".

B. I'm very familiar with Blyth. Unfortunately for your argument, Blyth was guided by typological thinking regarding animal populations. He saw each species as having a 'norm', from which it could not deviate. That is why he saw natural slection as a conservative force. Darwin, on the other hand recognized that there was no typological 'norm'--instead, species were actually continuums of variation.This of course, is the more accurate assessment. Look to the Drosophila paulistorum species complex for an exquisite example.

C) Your point here makes it clear you comprehended neither Miller's nor my point. Accumulated changes in allelic frequencies between populations produce differentiation that results in genetic incompatibilities which produce speciation. You dont have to have doctoral dissertation to comprehend that, and you can see the observed results of it here:

Dobzhansky, T. and O. Pavlovsky. 1971. Experimentally created incipient species of Drosophila. Nature. 230:289-292


d) Nowhere did I say divergence and variation are unlimited.You, on the other hand, keep saying that there are limits to this variatoon and what it can produce. I'd appreciate seeing your analysis and references showing exactly where the limitations are.

e) "As far as citing my research, I have cited Miller's research, he is a reputable scientist, and shown, by his own words, that he was erroneous in his conclusions. "

Please show us where Miller has ever done research with peppered moths. As for your research, I was asking for YOU to cite any relevant literature that makes your point.

(edited to add 'e")
Cheers,

KC

[ July 24, 2002: Message edited by: KCdgw ]</p>

KC

Jfoard writes: Ah, so you are familiar with Haldane's work? Could you please explain to us just what those assumptions were, and how they apply to natural populations, to justify your application of Haldane's figures to the human chimp divergence?

Thanks,

KC

scigirl

Jfoard,

A point of clarification about "good" and "bad" mutations: Here's a thought experiment for you.

If a mutation changed a person's immune system by increasing the amount of T cells (this could happen by making the promotor of the T cell growth factor more likely to bind to a transcription factor), would this be a "good" or a "bad" mutation?

scigirl

(Hint - "good" and "bad" is a silly way to think about biology, and the answer you give will depend on the context).

[ July 24, 2002: Message edited by: scigirl ]</p>

KC

Bumping this one up, lest we forget about it.

KC

Tharmas

Found <a href="http://www.gate.net/~rwms/hald_contents.html" target="_blank"> this web page</a>about Haldane's dilemma. Seems to cover the topic pretty well.
[edited to add the conclusion of the above-mentioned website]:

[ July 30, 2002: Message edited by: Tharmas ]</p>