Characterization of the response to circadian stress in Arabidopsis thaliana

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The objective of this grant proposal is to study a recently discovered novel type of abiotic stress in plants, which has been named circadian stress. Circadian stress occurs upon changes of the light-dark rhythm and has been first observed in cytokinin-deficient Arabidopsis thaliana plants which showed particularly strong stress symptoms. This indicated that cytokinin is required to protect plants from this type of stress. The circadian stress symptoms include deregulated expression of numerous stress response genes, a reduced photosynthetic activity, a strong increase of the jasmonic acid content and eventually programmed cell death in leaves. Stress symptoms were strongly alleviated in a genetic background with reduced jasmonic acid synthesis showing that the increase in this hormone is causal for inducing circadian stress symptoms. Various circadian clock mutants, in particular those with an abolished or reduced activity of the morning genes CCA1 and LHY, are highly sensitive to circadian stress. This shows that a well-functioning clock is important to respond to circadian stress and led to the hypothesis that circadian stress conditions push the normally well-balanced clock to its limit. Studying the circadian stress syndrome will be informative about the functioning of the circadian clock in plants, about the role of cytokinin in stabilizing clock function and about mechanisms normally preventing or dampening clock-generated stress signals. The project is divided into three parts. In the first part a number of basic questions will be answered such as: Which other tissues than leaves are responding to circadian stress? When do plants become competent to respond to circadian stress? Which changes occur in the metabolome after a circadian stress treatment? Which other hormones are involved in regulating the response to circadian stress? And finally, what are the links between cytokinin and the circadian clock? In a second part we will study in detail the roles of jasmonic acid and reactive oxygen species (ROS) signaling in causing programmed cell death upon circadian stress. In the third part we aim to get deeper insight into the molecular mechanisms involved in the response to circadian stress by identifying new components involved in generating or preventing the circadian stress syndrome. One approach to identify candidate genes is to study the transcriptomic response profile and its dynamics. Last but not least genetic screens are proposed aiming to identify mutants showing altered stress responses and to clone the corresponding genes. Together, a profound analysis of the molecular and the genetic mechanisms underlying the circadian stress phenotype will be performed to contribute to a better understanding of the circadian stress syndrome.