Signaling Meeting Minutes July 2009
13th July 2009
Participants: Nicolas Le Novere, Alex Diehl, Ruth Lovering, Peter D'Eustachio, Stan Lauderkind, Harold Drabkin, Sandra Orchard, Val Wood, Susan Tweedie.
Chair: Jennifer Deegan
Minutes: Jennifer Deegan
- Demo of new top term structure.
- Which areas of signaling in GO most urgently need attention?
- Does anybody have time to meet for one hour a week to work on edits?
Questions raised by Nicolas Le Novere:
Some of the issues I wanted to bring on were:
1) "neuronal signal transduction" is_a "signal transduction via ionic flux".
This is not correct, and translates the fact that one term describes a phenomenon at the molecular level, while the other describes a phenomenon at the cellular level. First it is not clear what "neuronal signal transduction" means. Is-it a neuron that transduces the signal coming from other neurons to its targets (including signal propagation and integration)? Or is-it the transduction of the signal sent by a neuron to the next? For the latter, there are plenty of different types: Volume transmission, wired transmission, that itself can be through an electrical synapse, a chemical synapse etc. A chemical synapse can in turn use ligand-gated ionic channels, GPCR, growth factors receptors etc.
2) "signal transduction via ionic flux"
I believe this term is overloaded and does not represent what you meant. A ionic flux is just another type of diffusible mediator. Think about calcium for instance. This is presumably not what was intended here. What we need to have is something like:
"signal transduction via the change of an environment parameter"
It could have the following children:
"signal transduction via the change of membrane polarisation" "signal transduction via the change of osmotic pressure" "signal transduction via the change of pH"
3) I still think that beside the diffusible mediator and the environment parameter, we need two other types:
"signal transduction via conformational change", as it is the case for the upper part of GPCR cascade for instance. But also much of the signal transduction involved in cellular movement, deformation, etc.
Something like "signal transduction via clustering". This is how all the growth factor receptors function. Once activated (generally through phosphorylation, itself brought by clustering of the receptors), they cause the aggregation of downstream targets, increasing their local concentration and causing signal propagation. Examples are EGFR, NGFR, TGFbR etc.
Do-we need something like
"signal transduction via covalent modification"? The phosphorylations are generally only a way to get a conformational change or to create a handle for clustering.