Journal
MOLECULAR PLANT
Volume 8, Issue 9, Pages 1350-1365Publisher
CELL PRESS
DOI: 10.1016/j.molp.2015.04.008
Keywords
phytohormone cross talk; S-nitrosoglutathione reductase (GSNOR); S-nitrosylation; auxin signaling; auxin transport; Arabidopsis
Categories
Funding
- Natural Science Foundation of China [31371401]
- Qianjiang Talent Program of Zhejiang Province [2013R10074]
- Natural Science Foundation of Zhejiang Province [LY12C14001]
- Ministry of Human Resources and Social Security of China [ZC304013131]
- National Science Foundation of China [91317304, 31370313]
- National Science Foundation [IOS-1238812]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1238812] Funding Source: National Science Foundation
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Cross talk between phytohormones, nitric oxide (NO), and auxin has been implicated in the control of plant growth and development. Two recent reports indicate that NO promoted auxin signaling but inhibited auxin transport probably through S-nitrosylation. However, genetic evidence for the effect of S-nitrosylation on auxin physiology has been lacking. In this study, we used a genetic approach to understand the broader role of S-nitrosylation in auxin physiology in Arabidopsis. We compared auxin signaling and transport in Col-0 and gsnor1-3, a loss-of-function GSNOR1 mutant defective in protein de-nitrosylation. Our results showed that auxin signaling was impaired in the gsnor1-3 mutant as revealed by significantly reduced DR5-GUS/DR5-GFP accumulation and compromised degradation of AXR3NT-GUS, a useful reporter in interrogating auxin-mediated degradation of Aux/IAA by auxin receptors. In addition, polar auxin transport was compromised in gsnor1-3, which was correlated with universally reduced levels of PIN or GFP-PIN proteins in the roots of the mutant in a manner independent of transcription and 26S proteasome degradation. Our results suggest that S-nitrosylation and GSNOR1-mediated de-nitrosylation contribute to auxin physiology, and impaired auxin signaling and compromised auxin transport are responsible for the auxin-related morphological phenotypes displayed by the gsnor1-3 mutant.
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