期刊
PLANT CELL AND ENVIRONMENT
卷 38, 期 2, 页码 331-348出版社
WILEY
DOI: 10.1111/pce.12295
关键词
cell death; cryptogein; defence responses; histone deacetylase; NADPH oxidase; peroxynitrite; SnRK2 protein kinase
资金
- La Region de Bourgogne (PARI AGRALE 8 project)
- Association Pour la Recherche sur les Nicotianees
Nitric oxide (NO) has many functions in plants. Here, we investigated its interplays with reactive oxygen species (ROS) in the defence responses triggered by the elicitin cryptogein. The production of NO induced by cryptogein in tobacco cells was partly regulated through a ROS-dependent pathway involving the NADPH oxidase NtRBOHD. In turn, NO down-regulated the level of H2O2. Both NO and ROS synthesis appeared to be under the control of type-2 histone deacetylases acting as negative regulators of cell death. Occurrence of an interplay between NO and ROS was further supported by the finding that cryptogein triggered a production of peroxynitrite (ONOO-). Next, we showed that ROS, but not NO, negatively regulate the intensity of activity of the cryptogein-induced protein kinase NtOSAK. Furthermore, using a DNA microarray approach, we identified 15 genes early induced by cryptogein via NO. A part of these genes was also modulated by ROS and encoded proteins showing sequence identity to ubiquitin ligases. Their expression appeared to be negatively regulated by ONOO-, suggesting that ONOO- mitigates the effects of NO and ROS. Finally, we provided evidence that NO required NtRBOHD activity for inducing cell death, thus confirming previous assumption that ROS channel NO through cell death pathways. The interplays between nitric oxide ( NO ) and reactive oxygen species ( ROS ) in the defense responses triggered by the elicitin cryptogein in tobacco cells were investigated. Both NO and ROS resulting from NADPH oxidase activity contribute to cryptogein-induced cell death and regulate the expression of genes encoding ubiquitine ligases. In turn, peroxynitrite mitigates the effects of NO and ROS .
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