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Epidermal Cell Death in Rice Is Confined to Cells with a Distinct Molecular Identity and Is Mediated by Ethylene and H₂O₂ through an Autoamplified Signal Pathway^[W]

Botanisches Institut, Universität Kiel, 24118 Kiel, Germany

¹ Address correspondence to msauter{at}bot.uni-kiel.de.

Rice (Oryza sativa) forms adventitious root primordia at stem nodes during normal development. Root emergence is preceded by ethylene-induced, H₂O₂-mediated local death of epidermal cells. Exogenous H₂O₂ or enhancement of endogenous H₂O₂ promoted epidermal cell death in a dose-dependent manner. Inhibition of NADPH oxidase lowered ethylene-induced cell death rates. Inhibition of ethylene perception by 1-methylcyclopropene did not abolish H₂O₂-induced cell death, indicating that H₂O₂ acts downstream of ethylene. Microarray studies of epidermal cells that undergo cell death identified 61 genes coregulated by the ethylene-releasing compound ethephon and by H₂O₂, supporting a joint signaling pathway. Regulation of the ethylene biosynthetic genes 1-Aminocyclopropane-1-Carboxylate Oxidase1 and Ethylene Overproducer-Like1 and downregulation of Metallothionein2b (MT2b), which encodes a reactive oxygen scavenger, indicated mutual enhancement of ethylene and H₂O₂ signaling. Analysis of MT2b knockdown mutants showed that cell death rates were inversely related to MT2b transcript abundance. Epidermal cells above adventitious roots have a morphological and molecular identity distinct from other epidermal cells. Pro-death signals regulated several transcription factor genes with a proposed function in cell type specification. It is hypothesized that induction of cell death is dependent on epidermal cell identity.

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