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首页> 外文期刊>Journal of cell biology >Formation of cristae and crista junctions in mitochondria depends on antagonism between Fcj1 and Su e/g
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Formation of cristae and crista junctions in mitochondria depends on antagonism between Fcj1 and Su e/g

机译:线粒体中ista和ista连接的形成取决于Fcj1和Su e / g之间的拮抗作用

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摘要

Crista junctions (CJs) are important for mitochondrial organization and function, but the molecular basis of their formation and architecture is obscure. We have identified and characterized a mitochondrial membrane protein in yeast, Fcj1 (formation of CJ protein 1), which is specifically enriched in CJs. Cells lacking Fcj1 lack CJs, exhibit concentric stacks of inner membrane in the mitochondrial matrix, and show increased levels of F1FO–ATP synthase (F1FO) supercomplexes. Overexpression of Fcj1 leads to increased CJ formation, branching of cristae, enlargement of CJ diameter, and reduced levels of F1FO supercomplexes. Impairment of F1FO oligomer formation by deletion of its subunits e / g (Su e / g ) causes CJ diameter enlargement and reduction of cristae tip numbers and promotes cristae branching. Fcj1 and Su e / g genetically interact. We propose a model in which the antagonism between Fcj1 and Su e / g locally modulates the F1FO oligomeric state, thereby controlling membrane curvature of cristae to generate CJs and cristae tips.
机译:crista连接(CJs)对于线粒体的组织和功能很重要,但其形成和结构的分子基础尚不清楚。我们已经鉴定并鉴定了酵母中的线粒体膜蛋白Fcj1(CJ蛋白1的形成),它特别富含CJs。缺乏Fcj1的细胞缺乏CJ,在线粒体基质中显示同心的内膜堆叠,并显示出水平升高的F1FO–ATP合酶(F1FO)超复合物。 Fcj1的过度表达导致CJ形成增加,cr分支,CJ直径增大和F1FO超复合物水平降低。通过删除其亚基e / g(Su e / g)来破坏F1FO低聚物的形成会导致CJ直径增大和of尖端数减少,并促进cr分支。 Fcj1与Su e / g发生基因相互作用。我们提出了一个模型,其中Fcj1与Su e / g之间的拮抗作用局部调节F1FO的寡聚状态,从而控制of的膜曲率以生成CJ和cr尖端。

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