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Oilseed rape NAC56 transcription factor modulates reactive oxygen species accumulation and hypersensitive response‐like cell death
Author(s) -
Chen Qinqin,
Niu Fangfang,
Yan Jingli,
Chen Bisi,
Wu Feifei,
Guo Xiaohua,
Yang Bo,
Jiang YuanQing
Publication year - 2017
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/ppl.12545
Subject(s) - reactive oxygen species , transcription factor , biology , programmed cell death , microbiology and biotechnology , hypersensitive response , jasmonic acid , abscisic acid , wrky protein domain , activator (genetics) , gene expression , gene , biochemistry , transcriptome , apoptosis
The NAC ( NAM , ATAF1 /2, CUC2 ) transcription factor gene family is plant‐specific and plays diverse roles in development and responses to abiotic stresses and pathogen challenge. Oilseed rape ( Brassica napus ) or canola is an important oil crop worldwide, however, the function of NAC genes in it remains largely elusive. In the present study, we identified and characterized the NAC56 gene isolated from oilseed rape. Expression of BnaNAC56 was induced by abscisic acid ( ABA ), jasmonic acid ( JA ), methyl viologen ( MV ) and a necrotrophic fungal pathogen Sclerotinia sclerotiorum , but repressed by cold. BnaNAC56 is a transcription activator and localized to nuclei. Overexpression of BnaNAC56 induced reactive oxygen species ( ROS ) accumulation and hypersensitive response ( HR )‐like cell death, with various physiological measurements supporting these. Furthermore, BnaNAC56 expression caused evident nuclear DNA fragmentation. Moreover, quantitative reverse transcription PCR ( qRT‐PCR ) analysis identified that the expression levels of multiple genes regulating ROS homeostasis, cell death and defense response were significantly induced. Using a dual luciferase reporter assay, we further confirmed that BnaNAC56 could activate the expression of a few ROS ‐ and cell death‐related genes. In summary, our data demonstrate that BnaNAC56 functions as a stress‐responsive transcriptional activator and plays a role in modulating ROS accumulation and cell death.