Characterization of a novel salt stress signaling component

High soil salinity is detrimental for plant growth and development and severely affects agronomical yield. Plants respond to high salt conditions via complex mechanisms, including physiological and biochemical adjustments. This multitude of stress-induced responses is delicately coordinated by a network of signal transduction pathways ultimately determining whether a plant is able to acclimate. Although detailed knowledge about the molecular mechanisms of high salt signaling is of great significance, our understanding of salt induced signal transduction is still limited. In our recent work, we discovered the Arabidopsis protein kinase ASKalfa as novel regulator of salt stress tolerance. ASKalfa is post-translationally activated by high salinity conditions. Plants deficient in ASKalfa are hypersensitive while plants with enhanced ASKalfa activity are more tolerant to salt stress. Furthermore, we identified an enzyme involved in regulating the cellular redox balance as an in vivo substrate of ASKalfa. Having established a key role of ASKalfa in modulating tolerance to high salt conditions we now aim to: (I) analyze how ASKalfa activity is regulated at the molecular level, (II) identify the upstream regulators of ASKalfa, and (III) identify and characterize additional stress-related targets of ASKalfa. We will combine molecular, genetic and biochemical techniques with physiological analyzes in Arabidopsis thaliana to address these aims and expect that this comprehensive approach will significantly increase our understanding of basic mechanisms of salt stress signaling and tolerance.

Unfavorable environmental conditions and pathogen infections limit plant growth and development and, thus, reduce agronomic yield. Plants have evolved complex cellular and physiological mechanisms to prevent damage and enable growth under stress conditions. These responses are controlled by different stress-type specific but also common and interacting signalling pathways, which may inhibit each other explaining the trade-off between biotic and abiotic stress responses. Interestingly, we discovered the protein kinase ASK? as a positive regulator of both abiotic and biotic stress tolerance of the model plant Arabidopsis. Plants deficient in ASK? are more sensitive to high soil salinity and are more susceptible to pathogen infection, whereas plants with increased ASK? activity are more resistant to salt stress and pathogen infection. Salt stress and pathogen infection enhance ASK? activity, which in turn enhances the activity of a key metabolic enzyme (glucose 6-phosphate dehydrogenase, G6PD). Remarkably, ASK?/G6PD have a dual role under abiotic and biotic stress conditions. Under salt stress, activation of G6PD induces the removal of excess levels of reactive oxygen species (ROS), which can lead to damage. However, after pathogen infection G6PD activity enhances the production of ROS, which is necessary for a successful immune response. Overall, our data provide evidence that ASK? and G6PD constitute a regulatory module that links signal transduction to metabolic adjustment under both abiotic and biotic stress conditions thus enabling plants to cope with diverse stresses.