Higuchi-Sanabria Ryo, Vevea Jason D, Charalel Joseph K, Sapar Maria L, Pon Liza A
Department of Pathology and Cell Biology, Columbia University, New York, NY, USA.
Department of Pathology and Cell Biology, Columbia University, New York, NY, USA. ; Current address: Department of Neuroscience, University of Wisconsin, Madison, WI, USA.
Microb Cell. 2016 Jan 18;3(2):79-88. doi: 10.15698/mic2016.02.478.
Increasing the stability or dynamics of the actin cytoskeleton can extend lifespan in and . Actin cables of budding yeast, bundles of actin filaments that mediate cargo transport, affect lifespan control through effects on mitochondrial quality control. Sir2p, the founding member of the Sirtuin family of lifespan regulators, also affects actin cable dynamics, assembly, and function in mitochondrial quality control. Here, we obtained evidence for novel interactions between Sir2p and Sum1p, a transcriptional repressor that was originally identified through mutations that genetically suppress ∆ phenotypes unrelated to lifespan. We find that deletion of in wild-type cells results in increased mitochondrial function and actin cable abundance. Furthermore, deletion of suppresses defects in actin cables and mitochondria of ∆ yeast, and extends the replicative lifespan and cellular health span of ∆ cells. Thus, Sum1p suppresses Sir2p function in control of specific aging determinants and lifespan in budding yeast.
增强肌动蛋白细胞骨架的稳定性或动力学可以延长[具体生物名称1]和[具体生物名称2]的寿命。芽殖酵母的肌动蛋白电缆，即介导货物运输的肌动蛋白丝束，通过影响线粒体质量控制来影响寿命调控。Sir2p是寿命调节因子Sirtuin家族的创始成员，它也影响肌动蛋白电缆的动力学、组装以及在线粒体质量控制中的功能。在这里，我们获得了Sir2p与Sum1p之间新相互作用的证据，Sum1p是一种转录抑制因子，最初是通过在与寿命无关的基因抑制Δ表型的突变中鉴定出来的。我们发现，在野生型细胞中缺失[相关基因名称]会导致线粒体功能增强和肌动蛋白电缆丰度增加。此外，缺失[相关基因名称]可抑制Δ酵母肌动蛋白电缆和线粒体的缺陷，并延长Δ细胞的复制寿命和细胞健康寿命。因此，Sum1p在芽殖酵母中控制特定衰老决定因素和寿命方面抑制Sir2p的功能。
