Stress-induced nuclear-to-cytoplasmic translocation of cyclin C promotes mitochondrial fission in yeast.
Stress-induced nuclear-to-cytoplasmic translocation of cyclin C promotes mitochondrial fission in yeast.
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DOI：
10.1016/j.devcel.2013.12.009
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发表时间：
2014-01-27
影响因子：
11.8
通讯作者：
Strich, Randy
中科院分区：
文献类型：
--
作者：
Cooper, Katrina F.;Khakhina, Svetlana;Kim, Stephen K.;Strich, Randy
线粒体的形态是由基于动力蛋白的分裂和融合机器的相反活动维持的。作为对压力的反应，这种平衡戏剧性地转向裂变。这项研究表明，酵母转录抑制因子细胞周期蛋白C是必要的和足够的压力诱导的超分裂。作为对氧化应激的反应，细胞周期蛋白C从细胞核转移到细胞质，在细胞质中被破坏。在其被破坏之前，细胞周期蛋白C在遗传和物理上都与Mdv1p相互作用，Mdv1p是一种将GTdR Dnm1p连接到线粒体受体Fis1p的接头。细胞周期蛋白C是所需的应激诱导Mdv1p线粒体招聘和功能Dnm1p丝的有效形成。最后，免疫共沉淀研究和荧光显微镜显示，在依赖于细胞周期蛋白C的应激细胞中，Mdv1p和Dnm1p之间的关联升高。本研究提供了一种机制，通过这种机制，应激诱导的基因诱导和线粒体分裂是通过细胞周期蛋白C的易位协调的。
Mitochondrial morphology is maintained by the opposing activities of dynamin-based fission and fusion machines. In response to stress, this balance is dramatically shifted toward fission. This study reveals that the yeast transcriptional repressor cyclin C is both necessary and sufficient for stress-induced hyper-fission. In response to oxidative stress, cyclin C translocates from the nucleus to the cytoplasm where it is destroyed. Prior to its destruction, cyclin C both genetically and physically interacts with Mdv1p, an adaptor that links the GTPase Dnm1p to the mitochondrial receptor Fis1p. Cyclin C is required for stress-induced Mdv1p mitochondrial recruitment and the efficient formation of functional Dnm1p filaments. Finally, co-immunoprecipitation studies and fluorescence microscopy revealed an elevated association between Mdv1p and Dnm1p in stressed cells that is dependent on cyclin C. This study provides a mechanism by which stress-induced gene induction and mitochondrial fission are coordinated through translocation of cyclin C.
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DOI：
10.1073/pnas.97.2.662
发表时间：
2000-01-18
影响因子：
11.1
作者：
Igaki, T;Kanuka, H;Miura, M
通讯作者：
Miura, M
影响因子：
21.3
作者：
Bleazard, W;McCaffery, JM;Shaw, JM
通讯作者：
Shaw, JM
影响因子：
11.8
作者：
Cerveny, Kara L.;Studer, Seth L.;Sesaki, Hiromi
通讯作者：
Sesaki, Hiromi
影响因子：
7.8
作者：
Hermann, G J;Thatcher, J W;Mills, J P;Hales, K G;Fuller, M T;Nunnari, J;Shaw, J M
通讯作者：
Shaw, J M
影响因子：
7.8
作者：
Karren, MA;Coonrod, EM;Shaw, JM
通讯作者：
Shaw, JM