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生长信号通过诱导抑制静止状态的超氧阴离子，促进出芽酵母的时序性衰老。

Growth signaling promotes chronological aging in budding yeast by inducing superoxide anions that inhibit quiescence.

作者信息

Weinberger Martin, Mesquita Ana, Caroll Timothy, Marks Laura, Yang Hui, Zhang Zhaojie, Ludovico Paula, Burhans William C

机构信息

Department of Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, NY 14263, USA.

出版信息

Aging (Albany NY). 2010 Oct;2(10):709-26. doi: 10.18632/aging.100215.

DOI:10.18632/aging.100215
PMID:21076178
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2993800/
Abstract

Inhibition of growth signaling pathways protects against aging and age-related diseases in parallel with reduced oxidative stress. The relationships between growth signaling, oxidative stress and aging remain unclear. Here we report that in Saccharomyces cerevisiae, alterations in growth signaling pathways impact levels of superoxide anions that promote chronological aging and inhibit growth arrest of stationary phase cells in G0/G1. Factors that decrease intracellular superoxide anions in parallel with enhanced longevity and more efficient G0/G1 arrest include genetic inactivation of growth signaling pathways that inhibit Rim15p, which activates oxidative stress responses, and downregulation of these pathways by caloric restriction. Caloric restriction also reduces superoxide anions independently of Rim15p by elevating levels of H₂O₂, which activates superoxide dismutases. In contrast, high glucose or mutations that activate growth signaling accelerate chronological aging in parallel with increased superoxide anions and reduced efficiency of stationary phase G0/G1 arrest. High glucose also activates DNA damage responses and preferentially kills stationary phase cells that fail to arrest growth in G0/G1. These findings suggest that growth signaling promotes chronological aging in budding yeast by elevating superoxide anions that inhibit quiescence and induce DNA replication stress. A similar mechanism likely contributes to aging and age-related diseases in complex eukaryotes.

摘要

生长信号通路的抑制可通过降低氧化应激来预防衰老和与年龄相关的疾病。生长信号、氧化应激与衰老之间的关系仍不清楚。在此，我们报道在酿酒酵母中，生长信号通路的改变会影响超氧阴离子水平，超氧阴离子会促进时序性衰老并抑制静止期细胞在G0/G1期的生长停滞。与延长寿命和更有效的G0/G1期停滞同时出现的、能降低细胞内超氧阴离子的因素包括抑制Rim15p的生长信号通路发生基因失活，Rim15p可激活氧化应激反应，以及通过热量限制下调这些通路。热量限制还可通过提高过氧化氢水平来独立于Rim15p降低超氧阴离子，过氧化氢可激活超氧化物歧化酶。相反，高糖或激活生长信号的突变会加速时序性衰老，同时超氧阴离子增加，静止期G0/G1期停滞的效率降低。高糖还会激活DNA损伤反应，并优先杀死那些在G0/G1期未能停止生长的静止期细胞。这些发现表明，生长信号通过提高抑制静止并诱导DNA复制应激的超氧阴离子水平来促进芽殖酵母的时序性衰老。类似的机制可能也导致了复杂真核生物的衰老和与年龄相关的疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/775385ae8d38/aging-02-709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/3ee6cbb1f01d/aging-02-709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/b4d430841e6c/aging-02-709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/fc315532f749/aging-02-709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/9282e18a1bd9/aging-02-709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/e983a5fd1a78/aging-02-709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/775385ae8d38/aging-02-709-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/3ee6cbb1f01d/aging-02-709-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/b4d430841e6c/aging-02-709-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/fc315532f749/aging-02-709-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/9282e18a1bd9/aging-02-709-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/e983a5fd1a78/aging-02-709-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aaa/2993800/775385ae8d38/aging-02-709-g006.jpg

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