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Fission yeast mitochondria are distributed by dynamic microtubules in a motor-independent manner

机译:裂变酵母线粒体由动态微管以独立于运动的方式分布

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The cytoskeleton plays a critical role in regulating mitochondria distribution. Similar to axonal mitochondria, the fission yeast mitochondria are distributed by the microtubule cytoskeleton, but this is regulated by a motor-independent mechanism depending on the microtubule associated protein mmb1p as the absence of mmb1p causes mitochondria aggregation. In this study, using a series of chimeric proteins to control the subcellular localization and motility of mitochondria, we show that a chimeric molecule containing a microtubule binding domain and the mitochondria outer membrane protein tom22p can restore the normal interconnected mitochondria network in mmb1-deletion (mmb1?) cells. In contrast, increasing the motility of mitochondria by using a chimeric molecule containing a kinesin motor domain and tom22p cannot rescue mitochondria aggregation defects in mmb1? cells. Intriguingly a chimeric molecule carrying an actin binding domain and tom22p results in mitochondria associated with actin filaments at the actomyosin ring during mitosis, leading to cytokinesis defects. These findings suggest that the passive motor-independent microtubule-based mechanism is the major contributor to mitochondria distribution in wild type fission yeast cells. Hence, we establish that attachment to microtubules, but not kinesin-dependent movement and the actin cytoskeleton, is required and crucial for proper mitochondria distribution in fission yeast.
机译:细胞骨架在调节线粒体分布中起关键作用。类似于轴突线粒体,裂变酵母线粒体由微管细胞骨架分布,但这取决于微管相关蛋白mmb1p​​的运动独立机制调节,因为缺乏mmb1p​​会引起线粒体聚集。在这项研究中,使用一系列嵌合蛋白控制线粒体的亚细胞定位和运动性,我们显示了包含微管结合域和线粒体外膜蛋白tom22p的嵌合分子可以恢复mmb1-deletion中正常的互连线粒体网络( mmb1?)单元格。相反,通过使用包含驱动蛋白运动域和tom22p的嵌合分子来增加线粒体的运动性不能挽救mmb1中的线粒体聚集缺陷。细胞。有趣的是,带有肌动蛋白结合结构域和tom22p的嵌合分子在有丝分裂期间导致与肌动蛋白环上肌动蛋白丝相关的线粒体,导致胞质分裂缺陷。这些发现表明,基于被动运动无关的微管的机制是野生型裂变酵母细胞中线粒体分布的主要贡献者。因此,我们建立了对微管的附着,而不是依赖于驱动蛋白的运动和肌动蛋白细胞骨架的附着,对于裂变酵母中正确的线粒体分布是必需的和至关重要的。

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