期刊
PLANT SCIENCE
卷 181, 期 5, 页码 540-544出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.plantsci.2011.04.004
关键词
S-nitrosylation; GSNOR; De-nitrosylation; Disease resistance; Plant defence response
资金
- BBSRC [BB/D011809/1]
- The Royal Society [Uf090321]
- HEC Pakistan
- Biotechnology and Biological Sciences Research Council [BB/D011809/1, BB/H000984/1] Funding Source: researchfish
- BBSRC [BB/D011809/1, BB/H000984/1] Funding Source: UKRI
A key feature of the plant defence response is the transient engagement of a nitrosative burst, resulting in the synthesis of reactive nitrogen intermediates (RNIs). Specific, highly reactive cysteine (Cys) residues of low pK(a) are a major site of action for these intermediates. The addition of an NO moiety to a Cys thiol to form an S-nitrosothiol (SNO), is termed S-nitrosylation. This redox-based post-translational modification is emerging as a key regulator of protein function in plant immunity. Here we highlight recent advances in our understanding of de-nitrosylation, the mechanism that depletes protein SNOs, with a focus on S-nitrosoglutathione reductase (GSNOR). This enzyme controls total cellular S-nitrosylation indirectly during the defence response by turning over S-nitrosoglutathione (GSNO), a major cache of NO bioactivity. Crown Copyright (C) 2011 Published by Elsevier Ireland Ltd. All rights reserved.
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