Network properties underlying seed germination control
Questions Study Group participants are asked to consider:
Can the light-promoted degradation of PIF lead to germination in the current biological model? Is any PIF-independent action of light required, or an unknown PIF-dependent action? What is the minimum number of light inputs?
GA levels are subject to DELLA-dependent feedback regulation. In seeds with high DELLA levels, GA levels should increase and DELLA levels should consequently decrease. So how could high levels of DELLA proteins be achieved in dark-treated seeds, and does this require the presence of further crucial components of the protein synthesis network? If so, what are their properties?
What are the most stable steady states. How close are these to germinating?
Could PIFs and ABA regulate GA metabolism simply by manipulating the DELLA-GA feedback loop?
Some groups insist that the GA/ABA interaction during germination takes place solely through the regulation of GA biosynthesis by ABA. Others have emphasised a GA-independent affect of ABA on DELLA protein stability. Can a model tell us which is most important?
The phenotypes of loss-of-function mutants have been described for all components of the proposed network. Can a model account for these?
Some parts of the network may be absent in some cells, and this may be compensated for by hormones from neighbouring cells. What happens if hormone influxes from neighbouring tissues are simulated?
Proceedings of the Mathematics in the Plant Sciences Study Group