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逆行信号与一种假定的金属蛋白酶之间的相互作用重新配置了质体的代谢和结构状态。

Reciprocity between a retrograde signal and a putative metalloprotease reconfigures plastidial metabolic and structural states.

作者信息

Wang Jin-Zheng, van de Ven Wilhelmina, Xiao Yanmei, He Xiang, Ke Haiyan, Yang Panyu, Dehesh Katayoon

机构信息

Institute for Integrative Genome Biology and Department of Botany and Plant Sciences, University of California, Riverside, Riverside, CA 92521, USA.

Department of Plant Biology, University of California, Davis, Davis, CA 95616, USA.

出版信息

Sci Adv. 2022 Jun 3;8(22):eabo0724. doi: 10.1126/sciadv.abo0724.

DOI:10.1126/sciadv.abo0724
PMID:35658042
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9166295/
Abstract

Reconfiguration of the plastidial proteome in response to environmental cues is central to tailoring adaptive responses. To define the underlying mechanisms and consequences of these reconfigurations, we performed a suppressor screen, using a mutant () accumulating high levels of a plastidial retrograde signaling metabolite, MEcPP. We isolated a revertant partially suppressing the dwarf stature and high salicylic acid of and identified the mutation in a putative plastidial metalloprotease (VIR3). Biochemical analyses showed increased VIR3 levels in , accompanied by reduced abundance of VIR3-target enzymes, ascorbate peroxidase, and glyceraldehyde 3-phophate dehydrogenase B. These proteomic shifts elicited increased HO, salicylic acid, and MEcPP levels, as well as stromule formation. High light recapitulated VIR3-associated reconfiguration of plastidial metabolic and structural states. These results establish a link between a plastidial stress-inducible retrograde signaling metabolite and a putative metalloprotease and reveal how the reciprocity between the two components modulates plastidial metabolic and structural states, shaping adaptive responses.

摘要

质体蛋白质组响应环境信号的重新配置是形成适应性反应的核心。为了确定这些重新配置的潜在机制和后果,我们使用了一个积累高水平质体逆行信号代谢物MEcPP的突变体进行了抑制子筛选。我们分离出了一个部分抑制该突变体矮小 stature 和高水杨酸水平的回复突变体,并鉴定出一个假定的质体金属蛋白酶(VIR3)中的突变。生化分析表明,该突变体中VIR3水平升高,同时VIR3靶向酶、抗坏血酸过氧化物酶和甘油醛-3-磷酸脱氢酶B的丰度降低。这些蛋白质组学变化导致过氧化氢、水杨酸和MEcPP水平升高,以及stromule形成。高光重现了VIR3相关的质体代谢和结构状态的重新配置。这些结果建立了质体应激诱导的逆行信号代谢物与假定金属蛋白酶之间的联系,并揭示了这两个成分之间的相互作用如何调节质体代谢和结构状态,从而形成适应性反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/f1ec0e389ad3/sciadv.abo0724-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/bb3801c86265/sciadv.abo0724-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/d1c1652a36b4/sciadv.abo0724-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/0407fb87823d/sciadv.abo0724-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/92a26c4a2127/sciadv.abo0724-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/aa2e02373c3c/sciadv.abo0724-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/e0a24bcb6c38/sciadv.abo0724-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/f1ec0e389ad3/sciadv.abo0724-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/bb3801c86265/sciadv.abo0724-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/d1c1652a36b4/sciadv.abo0724-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/0407fb87823d/sciadv.abo0724-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/92a26c4a2127/sciadv.abo0724-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/aa2e02373c3c/sciadv.abo0724-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/e0a24bcb6c38/sciadv.abo0724-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9a11/9166295/f1ec0e389ad3/sciadv.abo0724-f7.jpg

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