The maintenance of mitochondrial respiratory function and homeostasis is essential to human health. Here, we identify condensin II subunits as novel regulators of mitochondrial respiration and mitochondrial stress responses. Condensin II is present in the nucleus and cytoplasm. While the effects of condensin II depletion on nuclear genome organization are well studied, the effects on essential cytoplasmic and metabolic processes are not as well understood. Excitingly, we observe that condensin II chromosome-associated protein (CAP) subunits individually localize to different regions of mitochondria, suggesting possible mitochondrial-specific functions independent from those mediated by the canonical condensin II holocomplex. Changes in cellular ATP levels and mitochondrial respiration are observed in condensin II CAP subunit-deficient cells. Surprisingly, we find that loss of NCAPD3 also sensitizes cells to oxidative stress. Together, these studies identify new, and possibly independent, roles for condensin II CAP subunits in preventing mitochondrial damage and dysfunction. These findings reveal a new area of condensin protein research that could contribute to the identification of targets to treat diseases where aberrant function of condensin II proteins is implicated.

中文翻译：

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凝缩蛋白II蛋白功能障碍影响线粒体呼吸和线粒体氧化应激反应。

线粒体呼吸功能和体内平衡的维持对人体健康至关重要。在这里，我们确定凝聚素II亚基为线粒体呼吸和线粒体应激反应的新型调节剂。Condensin II存在于细胞核和细胞质中。虽然凝集素II耗竭对核基因组组织的影响已得到很好的研究，但对基本胞质和代谢过程的影响还没有被很好地理解。令人兴奋的是，我们观察到凝缩蛋白II染色体相关蛋白（CAP）亚基分别定位于线粒体的不同区域，提示可能的线粒体特异功能独立于经典的凝缩蛋白II全息复合体所介导的功能。在凝集素II CAP亚基缺陷细胞中观察到细胞ATP水平和线粒体呼吸的变化。令人惊讶地，我们发现NCAPD3的丧失也使细胞对氧化应激敏感。总之，这些研究确定了凝集素II CAP亚基在预防线粒体损伤和功能障碍中的新作用，并且可能是独立的。这些发现揭示了凝集素蛋白研究的新领域，该领域可能有助于鉴定治疗与凝集素II蛋白异常功能有关的疾病的靶标。