Calcium signalling in the chloroplast and in the regulation of nuclear gene expression

Abstract

Calcium is a universal second messenger involved in nearly every aspect of plant physiology and development. In response to a variety of biotic or abiotic stresses, calcium rapidly and transiently increases in the cytosol and in this way triggers the appropriate downstream response. To date, most of the research on calcium has focused on cytosolic calcium signalling, however recent advances have demonstrated that in the chloroplast Ca2+ concentrations are also controlled, and that chloroplast calcium signalling is involved in regulating the plant cell physiology.
This thesis describes work investigating both cytosolic and chloroplast calcium signalling, In the first case, I examined how cytosolic Ca2+ increases with different kinetics (Ca2+-signatures) can encode specific information, and how this can be translated into appropriate changes in transcript expression. To this aim, a dynamic mathematical model of the SA-mediated pathogen network was developed. Calcium is responsible for activating this defence pathway by a complex regulation of the components of this network. This model was able to predict fold-changes and kinetics of gene expression in response to any given calcium signature, hence it was able to accurately describe how specificity is encoded in plant cells. The properties emerging from this model provided insights into the mechanistic basis of calcium signature decoding.
Work on chloroplast calcium signalling focused on two different aspects. Firstly, the hypothesis that chloroplast calcium might regulate chloroplast gene expression was tested, and it was found to not be the case. Secondly, a new chloroplast-specific calcium response was discovered, in response to heat. Properties of this response were investigated, as well as its possible physiological functions. Finally, by using this calcium response as a readout, I addressed the question of heat-sensing in plants. Using this approach I discovered that there is a prominent role for membrane fluidity in controlling this heat-induced calcium increase.