scilosopher
Registered Senior Member
I mainly stole the phraseology of "meta" to describe an element of functional redundancy across a range of species, with potentially different molecular characteristics.
When I referred to networks I meant the regulatory links between factors (such as the protein from gene A activates transcription of gene B or the protein from gene X activates the protein from gene Y by phosphorylation).
The expression patterns generated by a network would therefore be a function of the regulatory interactions and the initial state of the system (including the distribution of various cell types expressing various different molecules).
I didn't intend to imply any experimental similarity between the Stuart paper and what I was suggesting. I meant mapping the functional interactions/regulatory links through a combination of misexpression, genetics, and biochemistry. All these are necessary to determine the various effects of molecules and more importantly the direct interactions responsible for those effects.
For instance removing a transcriptional repressor P can lead to LOSS of expression of gene R that is not even a target of that molecule. This could make one think P was an activator of R, when it is neither an activator or is R a target. Alternatively P could have been repressing Q, a direct repressor of R. Upon loss of P, Q is no longer repressed and therefore is expressed and can repress R.
Therefore one has to hunt down the molecular details of regulatory effects beyond a genetic description on effects upon expression patterns (although w/double mutants and detailed staging one can figure much out, but that's much more tricky and molecular handles make such inferences more straightforward to demonstrate).
When I referred to networks I meant the regulatory links between factors (such as the protein from gene A activates transcription of gene B or the protein from gene X activates the protein from gene Y by phosphorylation).
The expression patterns generated by a network would therefore be a function of the regulatory interactions and the initial state of the system (including the distribution of various cell types expressing various different molecules).
I didn't intend to imply any experimental similarity between the Stuart paper and what I was suggesting. I meant mapping the functional interactions/regulatory links through a combination of misexpression, genetics, and biochemistry. All these are necessary to determine the various effects of molecules and more importantly the direct interactions responsible for those effects.
For instance removing a transcriptional repressor P can lead to LOSS of expression of gene R that is not even a target of that molecule. This could make one think P was an activator of R, when it is neither an activator or is R a target. Alternatively P could have been repressing Q, a direct repressor of R. Upon loss of P, Q is no longer repressed and therefore is expressed and can repress R.
Therefore one has to hunt down the molecular details of regulatory effects beyond a genetic description on effects upon expression patterns (although w/double mutants and detailed staging one can figure much out, but that's much more tricky and molecular handles make such inferences more straightforward to demonstrate).