Circadian Stress Regimes Affect the Circadian Clock and Cause Jasmonic Acid-Dependent Cell Death in Cytokinin-Deficient Arabidopsis Plants

• Published in: The Plant cell Vol. 28; no. 7; pp. 1616 - 1639
• Main Authors: Nitschke, Silvia, Cortleven, Anne, Iven, Tim, Feussner, Ivo, Havaux, Michel, Riefler, Michael, Schmülling, Thomas
• Format: Journal Article
• Language: English
• Published: United States American Society of Plant Biologists 01.07.2016; American Society of Plant Biologists (ASPB)
• Subjects: Arabidopsis; Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Arabidopsis thaliana; Cell Death - genetics; Cell Death - physiology; Circadian Clocks - genetics; Circadian Clocks - physiology; Cyclopentanes - metabolism; Cytokinins - metabolism; DNA-Binding Proteins - genetics; DNA-Binding Proteins - metabolism; Gene Expression Regulation, Plant - genetics; Gene Expression Regulation, Plant - physiology; Life Sciences; Light; Oxylipins - metabolism; Reactive Oxygen Species - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism
• ISSN: 1040-4651; 1532-298X
• DOI: 10.1105/tpc.16.00016

The circadian clock helps plants measure daylength and adapt to changes in the day-night rhythm. We found that changes in the light-dark regime triggered stress responses, eventually leading to cell death, in leaves of Arabidopsis thaliana plants with reduced cytokinin levels or defective cytokinin signaling. Prolonged light treatment followed by a dark period induced stress and cell death marker genes while reducing photosynthetic efficiency. This response, called circadian stress, is also characterized by altered expression of clock and clock output genes. In particular, this treatment strongly reduced the expression of CIRCADIAN CLOCK ASSOCIATED1 (CCA1) and LATE ELONGATED HYPOCOTYL (LHY). Intriguingly, similar changes in gene expression and cell death were observed in clock mutants lacking proper CCA1 and LHY function. Circadian stress caused strong changes in reactive oxygen species- and jasmonic acid (JA)-related gene expression. The activation of the JA pathway, involving the accumulation of JA metabolites, was crucial for the induction of cell death, since the cell death phenotype was strongly reduced in the jasmonate resistant1 mutant background. We propose that adaptation to circadian stress regimes requires a normal cytokinin status which, acting primarily through the AHK3 receptor, supports circadian clock function to guard against the detrimental effects of circadian stress.