Mitochondrial retrograde signaling through UCP1-mediated inhibition of the plant oxygen-sensing pathway.
Mitochondrial retrograde signaling through UCP1-mediated inhibition of the plant oxygen-sensing pathway.
复制标题
线粒体逆行信号通过UCP1介导的植物氧感应途径的抑制。
DOI：
10.1016/j.cub.2022.01.037
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发表时间：
2022-03-28
期刊：
影响因子：
--
通讯作者：
Arruda P
中科院分区：
文献类型：
--
作者：
Barreto P;Dambire C;Sharma G;Vicente J;Osborne R;Yassitepe J;Gibbs DJ;Maia IG;Holdsworth MJ;Arruda P
线粒体逆行信号是真核生物细胞内应激信号的重要组成部分。解偶联蛋白（UncouplingProtein，UCP）1是一种丰富的植物线粒体内膜蛋白，具有解偶联呼吸和氨基酸转运等多种功能，广泛影响非生物胁迫反应。尽管这种逆行功能的作用机制尚不清楚，但UCP 1的过表达激活了缺氧（低氧）相关核基因的表达。在拟南芥中，我们发现UCP 1通过抑制蛋白水解（PRT）6 N-降解决定子途径的细胞质植物半胱氨酸氧化酶（PCO）分支（氧和一氧化氮（NO）传感的主要机制）影响核基因表达和生理反应。UCP 1（UCP 1 ox）的过表达导致人工PCO N-降解决定子途径底物的稳定，并且该报告蛋白的稳定性受到控制UCP 1活性的药理学干预的影响。在UCP 1 ox系中观察到的耐缺氧和耐盐表型与在PRT 6 N-识别素E3连接酶突变体prt 6 -1中观察到的表型相似。遗传分析表明，UCP 1调节缺氧反应需要PCO N-降解决定子途径乙烯反应因子（ERF）VII底物的活性。转录本表达分析表明，UCP 1对低氧相关基因表达的调控是幼苗发育的正常组成部分。我们的研究结果表明，线粒体逆行信号抑制PCO N-降解决定子途径，增强底物功能，从而促进下游应激反应。这项工作揭示了一种新的机制，通过线粒体逆行信号影响核反应缺氧抑制一个古老的细胞质途径的真核生物氧传感。UCP 1抑制PRT 6 N-降解决定子途径的PCO分支抑制导致底物稳定和基因表达改变抑制在发育过程中和对应激的反应中转导UCP 1功能Barreto等人。揭示了一种将线粒体内膜蛋白UCP 1与细胞质氧传感联系起来的逆行信号传导机制。UCP 1活性通过抑制PCO N-degron途径转导以影响基因表达。这种机制整合了发育过程中和应对压力时的线粒体和核功能。
Mitochondrial retrograde signaling is an important component of intracellular stress signaling in eukaryotes. UNCOUPLING PROTEIN (UCP)1 is an abundant plant inner-mitochondrial membrane protein with multiple functions including uncoupled respiration and amino-acid transport that influences broad abiotic stress responses. Although the mechanism(s) through which this retrograde function acts is unknown, overexpression of UCP1 activates expression of hypoxia (low oxygen)-associated nuclear genes. Here we show in Arabidopsis thaliana that UCP1 influences nuclear gene expression and physiological response by inhibiting the cytoplasmic PLANT CYSTEINE OXIDASE (PCO) branch of the PROTEOLYSIS (PRT)6 N-degron pathway, a major mechanism of oxygen and nitric oxide (NO) sensing. Overexpression of UCP1 (UCP1ox) resulted in the stabilization of an artificial PCO N-degron pathway substrate, and stability of this reporter protein was influenced by pharmacological interventions that control UCP1 activity. Hypoxia and salt-tolerant phenotypes observed in UCP1ox lines resembled those observed for the PRT6 N-recognin E3 ligase mutant prt6-1. Genetic analysis showed that UCP1 regulation of hypoxia responses required the activity of PCO N-degron pathway ETHYLENE RESPONSE FACTOR (ERF)VII substrates. Transcript expression analysis indicated that UCP1 regulation of hypoxia-related gene expression is a normal component of seedling development. Our results show that mitochondrial retrograde signaling represses the PCO N-degron pathway, enhancing substrate function, thus facilitating downstream stress responses. This work reveals a novel mechanism through which mitochondrial retrograde signaling influences nuclear response to hypoxia by inhibition of an ancient cytoplasmic pathway of eukaryotic oxygen sensing. UCP1 inhibits the PCO branch of the PRT6 N-degron pathway Inhibition leads to substrate stabilization and altered gene expression Inhibition transduces UCP1 function during development and in response to stress Barreto et al. uncover a retrograde signaling mechanism that links inner mitochondrial membrane protein UCP1 to cytoplasmic oxygen sensing. UCP1 activity is transduced via inhibition of the PCO N-degron pathway to influence gene expression. This mechanism integrates mitochondrial and nuclear functions during development and in response to stress.
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影响因子：
5.6
作者：
Barreto P;Yassitepe JECT;Wilson ZA;Arruda P
通讯作者：
Arruda P
DOI：
10.1073/pnas.1321892112
发表时间：
2014-12-30
影响因子：
11.1
作者：
Green, Peter T.;Harms, Kyle E.;Connell, Joseph H.
通讯作者：
Connell, Joseph H.
影响因子：
7.4
作者：
Lokdarshi, Ansul;Conner, W. Craig;Roberts, Daniel M.
通讯作者：
Roberts, Daniel M.
影响因子：
7.2
作者：
Clough, SJ;Bent, AF
通讯作者：
Bent, AF
影响因子：
7.2
作者：
Bui, Liem T.;Shukla, Vinay;Giuntoli, Beatrice
通讯作者：
Giuntoli, Beatrice