Dear all
Welcome to the 2008 departmental seminar series!
We kick off the year by welcoming a new member of department, Dr.
Karola Stotz
Karola will give her inaugural talk to the dept this Wed, at 3.30 in
The Refectory
Do come and make her welcome!
Also, of course, she'll be giving an introductory talk to graduate
students at 2PM in the Departmental Common Room -- all grad students
and anyone else who'd like to be introduced to the background of the
paper welcome (but grad student priority in question ansking!)
Title:
Molecular epigenesis: a postgenomic argument against Waters' thesis of
"causal specificity"
Abstract:
In a recent paper C. Kenneth Waters has presented an account of causal
reasoning in science that allows him to single out the 'cause' among
many 'conditions' and to argue against the notion that all causes are
on an ontological par. He therefore justifies the common biological
praxis to single out genes by describing the role of DNA as being
either the only, or at least the most important, causally specific
difference maker for the final sequence of gene products. In this
paper I want to show that while Waters analysis of the causal role of
genes is technically correct, by downplaying the causally specifying
role of gene regulatory mechanism against the role of DNA sequences
this analysis misses one of the most exiting points of postgenomic
research: what matters for an organims is less its number and sequence
of genes but the amplification of its gene products encoded in the
literal genetic code through complex gene expression mechanisms. These
provide a break with the central dogma of molecular genetics,
according to which sequence specificity for a gene product must be
template derived. In its place we find what is called here 'molecular
epigenesis' with its three classes of phenomena, sequence
'activation', 'selection' and 'creation'. Waters has also
misunderstood the philosophical 'parity thesis', which doesn't argue
against an ontological distinction between causes, but for the sharing
of distinct causal roles, such as sequence specificity, by quite
distinct developmental resources.
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