Re: Article: Unravelling new complexity in the genome
- From: "John W Edser" <edser@xxxxxxxxxxxxxx>
- Date: Wed, 15 Aug 2007 16:59:15 -0400 (EDT)
"Robert Karl Stonjek" <rstonjek@xxxxxxxxxxxxxx> wrote:-
A major surprise emerging from genome sequencing projects is that humans
have a comparable number of protein-coding genes as significantly less
complex organisms such as the minute nematode worm Caenorhabditis elegans.
Clearly something other than gene count is behind the genetic differences
between simpler and more complex life forms.
JE:-
I identify two "other than gene count " possibilities:-
1) CORRECTING non additive gene interactions from its present
status as "inherited" but not "heritable" to "inherited" and "heritable".
The
pioneering work of C. H. Waddington demonstrated over 50 years ago
that non additive gene associations remain heritable. His synthetic theory
( I posted Waddington's synthetic model twice to sbe) incorporated
this principle was based on two basic concepts:
a) Canalisation: a non additive incredibly higher rate of heritable,
phenotypic conservation.
b) Assimilation: a non additive amazingly rapid rate of heritable
phenotypic change.
Both remain ignored within today's synthetic models.
The high gearing of genetic epistasis provides the best of both words
for nature: higher rates of phenotypic conservation when things stay
the same and lightning fast rates of phenotypic change when things
change making the traditional model look like a model T ford. The
problem is non additive epistasis remains deleted from today's,
oversimplified, uncorrected, synthetic theory only because it was
inconvenient for the mathematics.
2) Actually incorporating and not just ignoring gene imprinting within
synthetic theory as a powerful above the gene (epigenetic) heritable
mechanism which can act as a fine tuner of the DNA/RNA system
allowing a parents adaptation to be passed on to offspring as an
epistatic set of genes in which some are inherited turned on and
others, turned off.
Increased functional and cellular complexity can be explained, in large
part, by how genes and the products of genes are regulated.
JE:-
Yes, where most regulation of one gene by another remains non additive
and therefore deleted within popular, uncorrected, oversimplified
Neo Darwinian models.
A University of
Toronto-led study published in the latest issue of Genome Biology reveals
that a step in gene expression (referred to as alternative splicing) is
more
highly regulated in a cell and tissue-specific manner than previously
appreciated and much of this additional regulation occurs in the nervous
system. The alternative splicing step allows a single gene to specify
multiple protein products by processing the RNA transcripts made from
genes
(which are translated to make protein).
JE:-
Such a massive non additive effect remains deleted from Neo Darwinian
models.
"We are finding that a significant number of genes operating in the same
biological processes and pathways are regulated by alternative splicing
differently in nervous system tissues compared to other mammalian
tissues,"
says lead investigator Professor Benjamin Blencowe of the Banting and Best
Department of Medical Research and Centre for Cellular and Biomolecular
Research (CCBR) at the University of Toronto
According to Blencowe, it is particularly interesting that many of the
genes
have important and specific functions in the nervous system, including
roles
associated with memory and learning. However, in most cases the
investigators working on these genes were not aware that their favorite
genes are regulated at the level of splicing. Blencowe believes that the
data his group has generated provides a valuable basis for understanding
molecular mechanisms by which genes can function differently in different
parts of the body.
JE:-
Leaving the gene centric theory dead in the water.
Blencowe attributes these new findings in part to the power of a new tool
that he, together with his colleagues including Profs. Brendan Frey
(Department of Electrical and Computer Engineering) and Timothy Hughes
(Banting and Best, CCBR), developed a few years ago. This tool, which
comprises tailored designed microarrays or "gene chips" and computer
algorithms, allows the simultaneous measurement of thousands of
alternative
splicing events in cells and tissues. "Until recently researchers studied
splicing regulation on a gene by gene basis. Now we can obtain a picture
of
what is happening on a global scale, which provides a fascinating new
perspective on how genes are regulated," Blencowe explains.
JE:
Suddenly the mechanism of non additive genetic epistasis has become
observable. The heritability of genetic epistasis is just the heritability
of
basic pattern no matter if some genes become added or deleted.
snip for brevity<
Thanks Robert,
Regards,
John Edser
Independent Researcher
edser@xxxxxxxxxxxxxx
.
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