Os NAC 2 positively affects salt‐induced cell death and binds to the Os AP 37 and Os COX 11 promoters

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.