OsNAC2 positively affects salt‐induced cell death and binds to the OsAP37 and OsCOX11 promoters

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Summary Plant development and adaptation to environmental stresses are intimately associated with programmed cell death ( PCD ). Although some of the mechanisms regulating PCD [e.g., accumulation of reactive oxygen species ( ROS )] are common among responses to different abiotic stresses, the pathways mediating salt‐induced PCD remain largely uncharacterized. Here we report that overexpression of Os NAC 2 , which encodes a plant‐specific transcription factor, promotes salt‐induced cell death accompanied by the loss of plasma membrane integrity, nuclear DNA fragmentation, and changes to caspase‐like activity. In Os NAC 2 ‐knockdown lines, cell death was markedly decreased in response to severe salt stress. Additionally, Os NAC 2 expression was enhanced in rice seedlings exposed to a high NaCl concentration. Moreover, the results of quantitative real‐time PCR , chromatin immunoprecipitation, dual‐luciferase, and yeast one‐hybrid assays indicated that Os NAC 2 targeted genes that encoded an ROS scavenger ( Os COX 11 ) and a caspase‐like protease ( Os AP 37 ). Furthermore, K + ‐efflux channels ( Os GORK and Os SKOR ) were clearly activated by Os NAC 2. Overall, our results suggested that Os NAC 2 accelerates NaCl‐induced PCD and provide new insights into the mechanisms that affect ROS accumulation, plant caspase‐like activity, and K + efflux.