The following essay is a few years old but still looks useful:
http://www.glenn.morton.btinternet.co.uk/gencode.htm
Jim Hofmann
Philosophy Department and Liberal Studies Program
California State University Fullerton
http://nsmserver2.fullerton.edu/departments/chemistry/evolution_creation/web
-----Original Message-----
From: bivalve [mailto:bivalve@mail.davidson.alumlink.com]
Sent: Thursday, October 18, 2001 9:31 AM
To: asa@calvin.edu; webmaster@discovery.org
Subject: Details on universal code claims, from Re: NCSE Contacts
Every Living Scientist (fwd)....Discovery Institute's reply
>><< surrounds the quotes from the one DI reply, DC:
precedes my replies.
>>In his press release, Miller writes:
"Look closely at the figure from this paper, and you'll see
something remarkable. The variations from the standard
code occur in regular patterns that can be traced directly
back to the standard code, which sits at the center of the
diagram."
This is false. The variant codes do not "occur in regular
patterns," but appear independently in unrelated lineages.
<<
DC: The problem here is what is regular. The change from
the universal code to the variants is regular in the sense
that the changes proceed in an orderly evolutionary pattern.
The occurrence of these changes is erratic, as is to be
expected for the occurrence of mutations, and this is what
the DI insists is not orderly. However, there is a pattern in
that the changes generally occur in those situations where
changes would be selected for (GC mutational bias and
genome reduction).
>>In short, Miller completely misrepresents the Knight et al.
composite phylogeny. There is no "regular pattern" to the
variant codes that maps congruently onto phylogenetic
trees from other data. Thus, far from providing what Miller
calls "unexpected confirmation of the evolution of the code
from a single common ancestor," the pattern of variant
codes represents a puzzle for a single tree of life.<<
DC: Miller was not talking about the phylogeny, and
claiming that the variant codes represent a puzzle for a
single tree of life does misrepresent it.
>>In his press release, Miller writes:
"As evolutionary biologists were quick to realize, slight
differences in the genetic code are similar to differences
between the dialects of a single spoken language. The
differences in spelling and word meanings between the
American, Canadian, and British dialects of English reflect
a common origin. Exactly the same is true for the universal
language of DNA."
This is--at best--a wildly inaccurate analogy. From context
and other clues, English speakers can discern that the
words "center" and "centre," or "color" and "colour," refer to
the same object. Meaning is preserved by context, and the
reader moves along without a hitch.
But a gene sequence from a ciliated protozoan such as
Tetrahymena (for instance), with the codons UAA and UAG
in its open reading frame (ORF), cannot be interpreted
correctly by the translation machinery of other eukaryotes
having the so-called "universal" code. <<
DC: Unless there is no difference in inferential ability
between readers of English and ribosomes, there is a flaw
in the DI interpretation.
>>Indeed, for two decades (see below), it was exactly this
deeply-embedded feature of the genetic code that led to
strong predictions about its necessary universality across
all organisms. It was widely thought that any change to the
genetic code of an organism would affect all the proteins
produced by that organism, leading to deleterious
consequences (e.g., truncated or misfolded proteins) or
lethality. Once the code evolved in the progenitor of all life, it
"froze," and all subsequent organisms would carry that
code. <<
DC: Yes, but those decades were not the last two. The
codon-capture hypothesis, proposed in 1985, provides an
evolutionary mechanism for departure from the universal
code.
>>In his press release, Miller writes:
"...the entire biotechnology industry is built upon the
universality of the genetic code. Genetically-modified
organisms are routinely created in the lab by swapping
genes between bacteria, plants, animals, and viruses. If
the coded instructions in those genes were truly as
different as the critics of evolution would have you believe,
none of these manipulations would work."
But some manipulations--namely, those involving
organisms with variant codes--do not work, unless the
researchers themselves intervene to ensure function. <<
DC: The deviations typically involve rare codons, so that the
manipulation might work. Only if a variant codon happens
to be placed in a crucial position and the new code is an
inadequate substitute (the latter situation highly likely if it is
a change to a stop codon but less so if it is another amino
acid) will the change be significant.
>>Consider, for instance, the release factor from the ciliate
Tetrahymena thermophila. Release factors (in eukaryotes,
these proteins are abbreviated as "eRF" to distinguish
them from prokaryotic release factors) catalyze the
separation of completed polypeptide chains (nascent
proteins) from the ribosomal machinery. Unlike other
eukaryotic release factors, however, that recognize all three
stop codons (UAA, UGA, and UAG), the Tetrahymena
thermophila release factor recognizes only the UGA codon
as "stop."
In 1999, Andrew Karamyshev and colleagues at the
University of Tokyo isolated the release factor (Tt-eRF1)
from Tetrahymena thermophila. But in order to express and
purify the protein, Karamyshev et al. had to manipulate it
genetically first. Why? The Tetrahymena thermophila gene
for Tt-eRF1 contains 10 codons in its open reading frame
that would be interpreted as "stop" by other
organisms--whereas Tetrahymena thermophila reads
these codons as glutamine:
"To express and purify the recombinant Tt-eRF1 protein
under heterologous expression conditions [i.e., in a cell
other than Tetrahymena--Karamyshev et al. used yeast
cells], 10 UAA/UAG triplets within the coding sequence
were changed to the glutamine codon CAA or CAG by
site-directed mutagenesis." [4]
Furthermore, Tt-eRF1 would not function when employed in
combination with ribosomes (translation machinery) from
other species:
"In spite of the overall conservative protein structure of
Tt-eRF1 compared with mammalian and yeast eRF1s, the
soluble recombinant Tt-eRF1 did not show any polypeptide
release activity in vitro using rat or Artemia ribosomes." [5]
Thus, when using an organism with a variant code
(Tetrahymena thermophila), researchers found that
They needed to modify (i.e., intelligently manipulate) the
gene sequences so that they could be expressed by other
organisms, and
They discovered that a key component of the genetic code
(namely, the release factor that terminates translation)
would not function properly with the translation machinery
of other organisms. <<
DC: This souds a bit inaccurate. UGA is still recognized by
Tetrahymena, so release could work with the right
sequence. However, it is also possible that in the billion or
so years since the split between ciliates and the
fungi-animal lineage, a few mutations have rendered parts
of the ribosomes incompatible.
>>Experiments to change the identity of transfer RNA
(tRNA)--another possible mechanism by which genetic
codes might reassign codon "meanings"--have shown that
the intermediate steps must be bridged by intelligent
(directed) manipulation. <<
DC: This is false, as shown by the example I cited in my
post on the universal code. Hemichordate mitochondria
have an intermediate stage between the universal code
and the modified code in echinoderm mitochondria. This
fits exactly with the evolutionary scenario proposed by the
codon capture hypothesis, which provides an undirected
change in tRNA identity. The archive of my post is at
http://www.calvin.edu/archive/asa/200110/0147.html
>>Please report any errors to webmaster@discovery.org
<<
DC: I am not sure if these are they types of errors this is
asking about, but am sending them anyway.
Dr. David Campbell
Old Seashells
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