From: colby@bu-bio.bu.edu (Chris Colby)
Newsgroups: talk.religion.misc,talk.origins
Subject: questions for super-biologist Antti
Date: 7 Sep 92 19:35:46 GMT
Followup-To: talk.origins
Organization: animal -- coelomate -- deuterostome

In article <1992Sep7.101512.25753@cs.joensuu.fi> asiivo@cs.joensuu.fi (Antti Siivonen) writes:

>	Common sense doesn't mean that you should be blind, on the contrary, 
>	you should examine things. At first, when evolution was introduced to 
>	me, I believed it. But the more I have studied the more suspicious I've
>	become.            

How much have you studied of evolution, Antti? Please demonstrate
your knowledge of evolution by answering the following questions.

1.) What is the Hardy-Weinberg equilibrium? How do you test for
deviations from it (what statistical test do you use) and what
can this tell you about the population in question?

2.) Imagine a heirarchical set of entities where the bottom level
of entities are self-reproducing. What criteria must be met for
natural selection to be operating at a level above the lowest?

3.) Explain how data concerning linkage disequilibrium in extant
populations can be used to infer selection. In the absense of
selection, how would linkage deteriorate over time (the equation
would be fine)?

4.) Explain how the examination of the level heterozygosity in a 
population can be a clue to if they are reproducing sexually or 
clonally.

5.) Imagine a biologist exposed 1000 bacterial plates to a selective. 
agent. The bacteria on the plates derived from 1000 separate cultures
started from a single clone. If mutations occurred at random with
respect to adaptive significance, what is the mathematical distribution
of mutants per plate you would expect to find? What distribution
would you find if adaptive mutations were induced by the selective 
agent? How would you rule out the selective agent simply being a 
generalized mutagen if the distribution differed from the one 
expected for random mutagenesis?

6.) Some types of natural selection do not result in a change
in allele frequency. Name two and how these are detected. Give
an example of each as detected either in the lab or wild. At
equilibrium, how can these be distinguished?

7.) What mechanisms have been proposed to explain the pattern of
nucleotide variation in repetitive DNA termed concerted evolution?
Are single repeats in orthologous gene families expected to be more 
or less divergent than orthologous single copy genes (if the rate of 
mutation is constant(*) for both) due to these mechanisms?

(*) in terms of mutation rate per nucleotide.

If you are really a biologist (yeah right) who has studied evolution
(uh huh, sure) and has found big flaws in it, you should at least
be able to answer these basic questions. The first one is fresh-
man level biology, the rest are somewhat harder. But, you have
claimed to be a better biologist than Darwin. I claim to be a
lesser biologist than Darwin, and I can easily answer them --
so you should have no trouble. Personally, I think you don't
have even the slightest grasp of evolutionary biology and your
objections stem solely from adherance to anti-scientific religious 
dogma.

P.S. You still haven't provided the references backing your claims
that A.) animal hybridization accompianied by changes in ploidy
have occurred (and explained it's relevance to speciation in the
plant genus _Tragopogon_) B.) "Point" birds in a flying wedge
suffer higher mortality (you haven't even addressed if there are
species where the point position is not shifting, much less why
this is incompatible with evolutionary biology.) I think you are
making these up (although I bet I could find an animal hyb experi-
ment that fits the bill if I looked) to fit your arguments.

>		Andreas - Siperian Sirri   Siberian Stint

Follow-ups to t.o.

Chris Colby 	---	 email: colby@bu-bio.bu.edu	---
"'My boy,' he said, 'you are descended from a long line of determined,
resourceful, microscopic tadpoles--champions every one.'"
 	--Kurt Vonnegut from "Galapagos"