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Os NAC 2 positively affects salt‐induced cell death and binds to the Os AP 37 and Os COX 11 promoters
Author(s) -
Mao Chanjuan,
Ding Jialin,
Zhang Bin,
Xi Dandan,
Ming Feng
Publication year - 2018
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.13867
Subject(s) - programmed cell death , chromatin immunoprecipitation , microbiology and biotechnology , reactive oxygen species , transcription factor , apoptosis , gene knockdown , biology , caspase , chemistry , promoter , biochemistry , gene expression , gene
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.