Stress-Induced Phenoptosis: Mechanistic Insights and Evolutionary Implications

被引:1
|
作者
Pandey, Taruna [1 ]
Ma, Dengke K. K. [1 ,2 ]
机构
[1] Univ Calif San Francisco, Cardiovasc Res Inst, Dept Physiol, San Francisco, CA 94143 USA
[2] Univ Calif Berkeley, Innovat Genom Inst, Berkeley, CA 94720 USA
基金
美国国家卫生研究院;
关键词
stress; phenoptosis; C; elegans; aging; organismic death; antagonistic pleiotropy; CELL-DEATH; OXIDATIVE STRESS; ELEGANS; HOST; APOPTOSIS; PROGRAM; PATHWAY;
D O I
10.1134/S0006297922120082
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Evolution by natural selection results in biological traits that enable organismic adaptation and survival under various stressful environments. External stresses can be sometimes too severe to overcome, leading to organismic death either because of failure in adapting to such stress, or alternatively, through a regulated form of organismic death (phenoptosis). While regulated cell deaths, including apoptosis, have been extensively studied, little is known about the molecular and cellular mechanisms underlying phenoptosis and its evolutionary significance for multicellular organisms. In this article, we review documented phenomena and mechanistic evidence emerging from studies of stress-induced phenoptosis in the multicellular organism C. elegans and stress-induced deaths at cellular levels in organisms ranging from bacteria to mammals, focusing on abiotic and pathogen stresses. Genes and signaling pathways involved in phenoptosis appear to promote organismic death during severe stress and aging, while conferring fitness and immune defense during mild stress and early life, consistent with their antagonistic pleiotropy actions. As cell apoptosis during development can shape tissues and organs, stress-induced phenoptosis may also contribute to possible benefits at the population level, through mechanisms including kin selection, abortive infection, and soma-to-germline resource allocation. Current models can generate experimentally testable predictions and conceptual frameworks with implications for understanding both stress-induced phenoptosis and natural aging.
引用
收藏
页码:1504 / 1511
页数:8
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