Sir2-independent life span extension by calorie restriction in yeast.
Sir2-independent life span extension by calorie restriction in yeast.
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DOI：
10.1371/journal.pbio.0020296
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发表时间：
2004-09
期刊：
影响因子：
9.8
通讯作者：
Kennedy BK
中科院分区：
文献类型：
--
作者：
Kaeberlein M;Kirkland KT;Fields S;Kennedy BK
热量限制减缓衰老，延长许多生物体的寿命。在酵母中，已经提出了一种机制解释，即热量限制通过激活Sir2来减缓衰老。在这里，我们报告了一个Sir2独立的途径，负责与热量限制相关的长寿效益的大部分。先前已经发现FOB1的缺失和SIR2的过表达通过降低衰老母细胞中毒性rDNA环的水平来延长寿命。我们发现，将卡路里限制与这些遗传干预措施中的任何一种相结合，可以显着延长寿命，从而产生迄今为止报道的最长寿的酵母菌株。此外，热量限制导致缺乏Sir2和Fob1的细胞比存在Sir2的细胞寿命延长。这些发现表明，Sir2和热量限制在平行的途径中起作用，以促进酵母和高等真核生物的长寿。这项研究表明，热量限制和Sir2通过不同的途径促进酵母的长寿。这破坏了公认的观点，并暗示了高等生物的衰老
Calorie restriction slows aging and increases life span in many organisms. In yeast, a mechanistic explanation has been proposed whereby calorie restriction slows aging by activating Sir2. Here we report the identification of a Sir2-independent pathway responsible for a majority of the longevity benefit associated with calorie restriction. Deletion of FOB1 and overexpression of SIR2 have been previously found to increase life span by reducing the levels of toxic rDNA circles in aged mother cells. We find that combining calorie restriction with either of these genetic interventions dramatically enhances longevity, resulting in the longest-lived yeast strain reported thus far. Further, calorie restriction results in a greater life span extension in cells lacking both Sir2 and Fob1 than in cells where Sir2 is present. These findings indicate that Sir2 and calorie restriction act in parallel pathways to promote longevity in yeast and, perhaps, higher eukaryotes. This study indicates that calorie restriction and Sir2 promote longevity in yeast through distinct pathways. This undermines the accepted view, and has implications for aging in higher organisms
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