Singlet oxygen produced from triplet excited chlorophylls in photosynthesis is a signal molecule that can induce programmed cell death (PCD) through the action of the OXIDATIVE STRESS INDUCIBLE 1 (OXI1) kinase. Here, we identify two negative regulators of light-induced PCD that modulate OXI1 expression: DAD1 and DAD2, homologs of the human antiapoptotic protein DEFENDER AGAINST CELL DEATH. Overexpressing OXI1 in Arabidopsis (Arabidopsis thaliana) increased plant sensitivity to high light and induced early senescence of mature leaves. Both phenomena rely on a marked accumulation of jasmonate and salicylate. DAD1 or DAD2 overexpression decreased OXI1 expression, jasmonate levels, and sensitivity to photooxidative stress. Knock-out mutants of DAD1 or DAD2 exhibited the opposite responses. Exogenous applications of jasmonate upregulated salicylate biosynthesis genes and caused leaf damage in wild-type plants but not in the salicylate biosynthesis mutant Salicylic acid induction-deficient2, indicating that salicylate plays a crucial role in PCD downstream of jasmonate. Treating plants with salicylate upregulated the DAD genes and downregulated OXI1 We conclude that OXI1 and DAD are antagonistic regulators of cell death through modulating jasmonate and salicylate levels. High light-induced PCD thus results from a tight control of the relative activities of these regulating proteins, with DAD exerting a negative feedback control on OXI1 expression.

Aix Marseille University Centre National de la Recherche Scientifique Commissariat à l'Energie Atomique et aux Energies Alternatives UMR 7265 Biosciences and Biotechnologies Institute of Aix Marseille CEA Cadarache F 13108 Saint Paul lès Durance France

Aix Marseille University Centre National de la Recherche Scientifique Commissariat à l'Energie Atomique et aux Energies Alternatives UMR 7265 Biosciences and Biotechnologies Institute of Aix Marseille CEA Cadarache F 13108 Saint Paul lès Durance France Université d'Avignon et des Pays de Vaucluse F 84000 Avignon France

Center for Desert Agriculture King Abdullah University of Science and Technology Thuwal Saudi Arabia

Institut Jean Pierre Bourgin Institut National de la Recherche Agronomique AgroParisTech Centre National de la Recherche Scientifique Université Paris Saclay F 78000 Versailles France

Laboratory of Growth Regulators Institute of Experimental Botany The Czech Academy of Sciences Palacký University CZ 78371 Olomouc Czech Republic

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$a OXI1 and DAD Regulate Light-Induced Cell Death Antagonistically through Jasmonate and Salicylate Levels / $c I. Beaugelin, A. Chevalier, S. D'Alessandro, B. Ksas, O. Novák, M. Strnad, C. Forzani, H. Hirt, M. Havaux, F. Monnet,

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$a Singlet oxygen produced from triplet excited chlorophylls in photosynthesis is a signal molecule that can induce programmed cell death (PCD) through the action of the OXIDATIVE STRESS INDUCIBLE 1 (OXI1) kinase. Here, we identify two negative regulators of light-induced PCD that modulate OXI1 expression: DAD1 and DAD2, homologs of the human antiapoptotic protein DEFENDER AGAINST CELL DEATH. Overexpressing OXI1 in Arabidopsis (Arabidopsis thaliana) increased plant sensitivity to high light and induced early senescence of mature leaves. Both phenomena rely on a marked accumulation of jasmonate and salicylate. DAD1 or DAD2 overexpression decreased OXI1 expression, jasmonate levels, and sensitivity to photooxidative stress. Knock-out mutants of DAD1 or DAD2 exhibited the opposite responses. Exogenous applications of jasmonate upregulated salicylate biosynthesis genes and caused leaf damage in wild-type plants but not in the salicylate biosynthesis mutant Salicylic acid induction-deficient2, indicating that salicylate plays a crucial role in PCD downstream of jasmonate. Treating plants with salicylate upregulated the DAD genes and downregulated OXI1 We conclude that OXI1 and DAD are antagonistic regulators of cell death through modulating jasmonate and salicylate levels. High light-induced PCD thus results from a tight control of the relative activities of these regulating proteins, with DAD exerting a negative feedback control on OXI1 expression.

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