Plant salt stress tolerance and oxidative signalling

High soil salinity is a major environmental constraint on plant growth and development in numerous places in the world, resulting in large reductions in agronomic yield. Plants have evolved mechanisms to develop tolerance to environmental stresses. These mechanisms include protein phosphorylation- and reactive oxygen species (ROS)- mediated signalling. Increased levels of ROS are produced when plants are challenged by stress. ROS are crucial for signal transduction (cellular information transfer) but, when accumulating to excess levels, can also induce oxidative stress and damage cells. Stress-induced protein phosphorylation rapidly alters the function of its target protein(s) which are often involved in signal transduction and physiological responses. Recent studies have significantly advanced our knowledge of high salinity stress signalling. Yet, our understanding of the molecular mechanisms behind the signal transduction resulting in salt-stress tolerance is still limited. The Arabidopsis protein kinase ASKa has recently been identified as an important regulator of salt stress tolerance by the lab of C. Jonak. ASKa is involved in maintaining the cellular redox balance and in detoxifying excess levels of ROS under salt stress conditions. Based on recent data showing that ROS induce ASKa activity, the proposed project seeks to investigate the interaction between ROS signalling and ASKa. The project will investigate the mechanism(s) by which ROS regulates the activity of ASKa and will study the role of ASKa in oxidative stress signalling and tolerance. Furthermore, this project will determine whether ASKa is involved in mediating tolerance to other types of abiotic stress, such as drought, heat, or freezing. To accomplish this, genetic, molecular, and biochemical approaches will be combined with physiological studies in the model plant Arabidopsis thaliana. Overall, this comprehensive study on the interaction between ROS signalling, ASKa, and redox homeostasis will significantly increase our understanding of the basic mechanisms underlying salt stress signalling and tolerance.

No additional funding sources recorded.