Aiyar Raeka S, Bohnert Maria, Duvezin-Caubet Stéphane, Voisset Cécile, Gagneur Julien, Fritsch Emilie S, Couplan Elodie, von der Malsburg Karina, Funaya Charlotta, Soubigou Flavie, Courtin Florence, Suresh Sundari, Kucharczyk Roza, Evrard Justine, Antony Claude, St Onge Robert P, Blondel Marc, di Rago Jean-Paul, van der Laan Martin, Steinmetz Lars M
European Molecular Biology Laboratory (EMBL), Genome Biology Unit, 69117 Heidelberg, Germany.
Institut für Biochemie und Molekularbiologie, ZBMZ, Universität Freiburg, 79104 Freiburg, Germany.
Nat Commun. 2014 Dec 18;5:5585. doi: 10.1038/ncomms6585.
Mitochondrial diseases are systemic, prevalent and often fatal; yet treatments remain scarce. Identifying molecular intervention points that can be therapeutically targeted remains a major challenge, which we confronted via a screening assay we developed. Using yeast models of mitochondrial ATP synthase disorders, we screened a drug repurposing library, and applied genomic and biochemical techniques to identify pathways of interest. Here we demonstrate that modulating the sorting of nuclear-encoded proteins into mitochondria, mediated by the TIM23 complex, proves therapeutic in both yeast and patient-derived cells exhibiting ATP synthase deficiency. Targeting TIM23-dependent protein sorting improves an array of phenotypes associated with ATP synthase disorders, including biogenesis and activity of the oxidative phosphorylation machinery. Our study establishes mitochondrial protein sorting as an intervention point for ATP synthase disorders, and because of the central role of this pathway in mitochondrial biogenesis, it holds broad value for the treatment of mitochondrial diseases.
线粒体疾病是全身性的,普遍存在且往往致命;然而治疗方法仍然稀缺。确定可作为治疗靶点的分子干预点仍然是一项重大挑战,我们通过自己开发的筛选试验来应对这一挑战。利用线粒体ATP合酶疾病的酵母模型,我们筛选了一个药物重新利用文库,并应用基因组学和生物化学技术来确定感兴趣的途径。在这里,我们证明,由TIM23复合体介导的调节核编码蛋白进入线粒体的分选过程,在酵母和表现出ATP合酶缺陷的患者来源细胞中都具有治疗作用。靶向依赖TIM23的蛋白分选可改善一系列与ATP合酶疾病相关的表型,包括氧化磷酸化机制的生物发生和活性。我们的研究确立了线粒体蛋白分选作为ATP合酶疾病的一个干预点,并且由于该途径在线粒体生物发生中的核心作用,它对线粒体疾病的治疗具有广泛的价值。