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.

Rice (Oryza sativa) forms adventitious root primordia at stem nodes during normal development. Root emergence is preceded by ethylene-induced, H(2)O(2)-mediated local death of epidermal cells. Exogenous H(2)O(2) or enhancement of endogenous H(2)O(2) 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 H(2)O(2)-induced cell death, indicating that H(2)O(2) 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 H(2)O(2), 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 H(2)O(2) 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.