"Cary Kittrell" <cary@afone.as.arizona.edu> wrote in message
news:cja0td$38r$1@oasis.ccit.arizona.edu...

In article <gB%5d.1404$En6.51619@news.uswest.net> "Atheist Crusher"
<Atheist@fools.com> writes:
<
<"Cary Kittrell" <cary@afone.as.arizona.edu> wrote in message
<news:cj9iq7$p3d$1@oasis.ccit.arizona.edu...
<> In article <rcW5d.8$301.22696@news.uswest.net> "Atheist Crusher"
<> <Atheist@fools.com> writes:
<> <

{...}

<> <That wasn't a bad effort for a drooling spastic with a rather large
hole
<> in
<> <its rather small head.
<> <Here , have mommy read this to you.
<> <
<> <When prominent biologists claim that "evolution is a fact", they are
<> stating
<> <a half-truth that means far less than what they would like the public
to
<> <believe. The theory states that the development of life is a purely
<> natural
<> <process, driven by known mechanisms. This is simply not true. There
is no
<> <evidence that life developed, or even could have developed, by a
purely
<> <natural process.
<> <
<> <http://www.ftrbooks.net/science/darwin/not_by_chance.htm
<>
<> Spetner's claim is that random mutations cannot lead to an increase
<> in genetic information.
<>
<> Experimental refutation at:
<>
<> http://nar.oupjournals.org/cgi/content/full/28/14/2794
<>
<>
<> -- cary
<And even more refutation to cover your refutation at:
<A Brief Look at the Evidence
<
<The Fossil Evidence. Evolution is supposed to be a process of change.

{...}

No. This one had nothing whatsoever to do with the topic at
hand, which is the supposed inability of random mutations
to result in an increase of information in the genome.

Quit changing the subject....
You atheists are so transparent.
It's about evolution ,but since you want to switch modes for the 9th out
of a ten possible threads here goes:
Evidence against the evolutionary explanation includes:

1.. There are five transposable elements on the pOAD2 plasmid. When
activated, transposase enzymes coded therein cause genetic recombination.
Externally imposed stress such as high temperature, exposure to a poison,
or starvation can activate transposases. The presence of the transposases
in such numbers on the plasmid suggests that the plasmid is designed to
adapt when the bacterium is under stress.

2.. All five transposable elements are identical, with 764 base pairs
(bp) each. This comprises over eight percent of the plasmid. How could
random mutations produce three new catalytic/degradative genes (coding for
EI, EII and EIII) without at least some changes being made to the
transposable elements? Negoro speculated that the transposable elements
must have been a 'late addition' to the plasmids to not have changed. But
there is no evidence for this, other than the circular reasoning that
supposedly random mutations generated the three enzymes and so they would
have changed the transposase genes if they had been in the plasmid all
along. Furthermore, the adaptation to nylon digestion does not take very
long (see point 5 below), so the addition of the transposable elements
afterwards cannot be seriously entertained.

3.. All three types of nylon degrading genes appear on plasmids and only
on plasmids. None appear on the main bacterial chromosomes of either
Flavobacterium or Pseudomonas. This does not look like some random origin
of these genes-the chance of this happening is low. If the genome of
Flavobacterium is about two million bp,7 and the pOAD2 plasmid comprises
45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the
total chromosomal DNA), then the chance of getting all three of the genes
on the pOAD2 plasmid would be about 0.0015. If we add the probability of
the nylon degrading genes of Pseudomonas also only being on plasmids, the
probability falls to 2.3 x 10-6. If the enzymes developed in the
independent laboratory-controlled adaptation experiments (see point 5,
below) also resulted in enzyme activity on plasmids (almost certainly, but
not yet determined), then attributing the development of the adaptive
enzymes purely to chance mutations becomes even more implausible.

4.. The antisense DNA strand of the four nylon genes investigated in
Flavobacterium and Pseudomonas lacks any stop codons.8 This is most
remarkable in a total of 1,535 bases. The probability of this happening by
chance in all four antisense sequences is about 1 in 1012. Furthermore,
the EIII gene in Pseudomonas is clearly not phylogenetically related to
the EII genes of Flavobacterium, so the lack of stop codons in the
antisense strands of all genes cannot be due to any commonality in the
genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid
is not necessary for the normal growth of Flavobacterium, so functionality
in the wild-type parent DNA sequences would appear not to be a factor in
keeping the reading frames open in the genes themselves, let alone the
antisense strands.

5.. http://www.answersingenesis.org/tj/v17/i3/bacteria.asp