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作 者:Vivek Dogra Rahul Mohan Singh Mengping Li Mingyue Li Somesh Singh Chanhong Kim
机构地区:[1]Shanghai Center for Plant Stress Biology,CAS Center for Excellence in Molecular Plant Sciences,Chinese Academy of Sciences,Shanghai 200032,China [2]University of the Chinese Academy of Sciences,Beijing 100049,China [3]Present address:Biotechnology Division,CSIR-Institute of Himalayan Bioresource Technology,Palampur 176061,India
出 处:《Molecular Plant》2022年第3期438-453,共16页分子植物(英文版)
基 金:This research was supported by the Strategic Priority Research Program from the Chinese Academy of Sciences(grant no.XDB27040102);the 100-Talent Program of the Chinese Academy of Sciences and the National Natural Science Foundation of China(NSFC)(grant no.31871397)to C.K.Support from a President's International Fellowship Initiative(PIFI)postdoctoral fellowship from the Chinese Academy of Sciences(no.2019PB0066)to V.D.is also acknowledged.
摘 要:Oxidative post-translational modifications of specific chloroplast proteins contribute to the initiation of retrograde signaling.The Arabidopsis thaliana EXECUTER1(EX1)protein,a chloroplast-localized singlet oxygen(^(1)O_(2))sensor,undergoes tryptophan(Trp)643 oxidation by^(1)O_(2),a chloroplast-derived and light-dependent reactive oxygen species.The indole side chain of Trp is vulnerable to^(1)O_(2),leading to the generation of oxidized Trp variants and priming EX1 for degradation by a membrane-bound FtsH protease.The perception of^(1)O_(2)via Trp643 oxidation and subsequent EX1 proteolysis facilitate chloroplast-to-nucleus retrograde signaling.In this study,we discovered that the EX1-like protein EX2 also undergoes^(1)O_(2)-dependent Trp530 oxidation and FtsH-dependent turnover,which attenuates^(1)O_(2)signaling by decelerating EX1-Trp643 oxidation and subsequent EX1 degradation.Consistent with this finding,the loss of EX2 function reinforces EX1-dependent retrograde signaling by accelerating EX1-Trp643 oxidation and subsequent EX1 proteolysis,whereas overexpression of EX2 produces molecular phenotypes opposite to those observed in the loss-of-function mutants of EX2.Intriguingly,phylogenetic analysis suggests that EX2 may have emerged evolutionarily to attenuate the sensitivity of EX1 toward^(1)O_(2).Collectively,these results suggest that EX2 functions as a negative regulator of the EX1 signalosome through its own^(1)O_(2)-dependent oxidation,providing a new mechanistic insight into the regulation of EX1-mediated^(1)O_(2)signaling.
关 键 词:EXECUTER1 EXECUTER2 singlet oxygen retrograde signaling Trp oxidation FtsH protease
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