Growth balance regulation by snrk1 under aba-stress conditions
In response to adverse environmental conditions, such as water scarcity, extreme temperatures or salinity plants trigger responses that promote stress tolerance and survival at the expense of growth. Despite the negative impact of stress on crop productivity how growth is modified by stress signalling pathways is largely unknown. One major component of the response to the most devastating stresses is ABA, a hormone that triggers cellular and whole-plant adaptive mechanisms via the activation of SnRK2 protein kinases. Another major player is the energy sensing SnRK1 protein kinase, which promotes plant stress tolerance and survival through the vast regulation of metabolism and gene expression. Preliminary results in the host lab have revealed deficient ABA responses in a partial SnRK1 loss-of-function mutant as well as the physical interaction between SnRK1 and the ABA-activated SnRK2 kinases, suggesting a functional connection between these two pathways. Furthermore, SnRK1 and SnRK2 have recently been implicated in the repression of a central growth regulator, the TOR (Target of Rapamycin) protein kinase. The aim of this proposal is to investigate the interaction between these two major stress-related kinases (SnRK1 and SnRK2) and to elucidate the mechanism(s) by which they modulate growth-promoting signalling pathways in response to ABA. To tackle the functional relevance of the SnRK1-SnRK2 connection, a combination of biochemical approaches, genetics, microscopy, cell-based assays and chemical genomics will be used. To identify growth regulators downstream of the SnRK axis, targeted analyses of TOR readouts will be employed in combination with unbiased analyses of SnRK1 interactors and substrates in ABA. Altogether this project will provide novel molecular insight on the trade-offs between stress tolerance and growth/yield that may potentially contribute to more successful crop improvement.