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Chloroplast Activity and 39phosphadenosine 59phosphate Signaling Regulate Programmed Cell Death in Arabidopsis1

Bibliography:

​Quentin Bruggeman, Christelle Mazubert, Florence Prunier, Raphaël Lugan, Kai Xun Chan, Su Yin Phua, Barry James Pogson, Anja Krieger-Liszkay, Marianne Delarue, Moussa Benhamed, Catherine Bergounioux, and Cécile Raynaud. Chloroplast Activity and 39phosphadenosine 59phosphate Signaling Regulate Programmed Cell Death in Arabidopsis1. Plant Physiology. doi: http:/​/​dx.​doi.​org/​10.​1104/​pp.​15.​01872

Authors:

Quentin Bruggeman, Christelle Mazubert, Florence Prunier, Raphaël Lugan, Kai Xun Chan, Su Yin Phua, Barry James Pogson, Anja Krieger-Liszkay, Marianne Delarue, Moussa Benhamed, Catherine Bergounioux, and Cécile Raynaud

Keywords:

N/A

Year:

2016

Abstract:

​Programmed cell death (PCD) is a crucial process both for plant development and responses to biotic and abiotic stress. There is accumulating evidence that chloroplasts may play a central role during plant PCD as for mitochondria in animal cells, but it is still unclear whether they participate in PCD onset, execution, or both. To tackle this question, we have analyzed the contribution of chloroplast function to the cell death phenotype of the myoinositol phosphate synthase1 (mips1) mutant that forms spontaneous lesions in a light-dependent manner. We show that photosynthetically active chloroplasts are required for PCD to occur in mips1, but this process is independent of the redox state of the chloroplast. Systematic genetic analyses with retrograde signaling mutants reveal that 39-phosphoadenosine 59-phosphate, a chloroplast retrograde signal that modulates nuclear gene expression in response to stress, can inhibit cell death and compromises plant innate immunity via inhibition of the RNA-processing 59-39 exoribonucleases. Our results provide evidence for the role of chloroplast-derived signal and RNAmetabolism in the control of cell death and biotic stress response.

ISSN:

0176-1617