Author
Listed:
- Jian Feng
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Graduate University of Chinese Academy of Sciences)
- Chun Wang
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Graduate University of Chinese Academy of Sciences)
- Qingguo Chen
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Graduate University of Chinese Academy of Sciences)
- Hui Chen
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences
Graduate University of Chinese Academy of Sciences)
- Bo Ren
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences)
- Xiaoming Li
(State Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences)
- Jianru Zuo
(State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences)
Abstract
Cytokinin is an essential phytohormone in plant growth and development. In Arabidopsis, cytokinin signalling is mediated by a phosphorelay that sequentially transfers phosphoryl groups from the cytokinin receptors to histidine phosphotransfer proteins (AHPs) and response regulators (ARRs). However, little is known about the regulatory mechanism of the phosphorelay. Here, we show that nitric oxide negatively regulates cytokinin signalling by inhibiting the phosphorelay activity through S-nitrosylation. S-nitrosylation of AHP1 at Cys 115 represses its phosphorylation and subsequent transfer of the phosphoryl group to ARR1. A non-nitrosylatable mutation of AHP1 renders the mutant protein insensitive to nitric oxide in repressing its phosphorylation, and partially relieves the inhibitory effect of nitric oxide on the cytokinin response. Conversely, a nitrosomimetic mutation of AHP1 causes reduced phosphorylation of AHP1 and ARR1, thereby resulting in a compromised cytokinin response. These findings illustrate a mechanism by which redox signalling and cytokinin signalling coordinate plant growth and development.
Suggested Citation
Jian Feng & Chun Wang & Qingguo Chen & Hui Chen & Bo Ren & Xiaoming Li & Jianru Zuo, 2013.
"S-nitrosylation of phosphotransfer proteins represses cytokinin signaling,"
Nature Communications, Nature, vol. 4(1), pages 1-9, June.
Handle:
RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2541
DOI: 10.1038/ncomms2541
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Cited by:
- Jian Zeng & Xin’Ai Zhao & Zhe Liang & Inés Hidalgo & Michael Gebert & Pengfei Fan & Christian Wenzl & Sebastian G. Gornik & Jan U. Lohmann, 2023.
"Nitric oxide controls shoot meristem activity via regulation of DNA methylation,"
Nature Communications, Nature, vol. 14(1), pages 1-13, December.
- Guochen Qin & Menghuan Qu & Bei Jia & Wei Wang & Zhuojun Luo & Chun-Peng Song & W. Andy Tao & Pengcheng Wang, 2023.
"FAT-switch-based quantitative S-nitrosoproteomics reveals a key role of GSNOR1 in regulating ER functions,"
Nature Communications, Nature, vol. 14(1), pages 1-15, December.
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