Aging

Aging in C. elegans involves measurable declines in morphology, reproduction, and behavior. Understanding the cellular and molecular processes leading to senescence in this nematode began in the early 1980s with the targeted identification of mutants that extended life span (an AGE phenotype). These studies identified at least two key regulators of life span, DAF-2, an insulin/IGF receptor ortholog, and DAF-16, a Forkhead-related transcription factor. Since then many more genes and pathways involved in senescence have been identified. Almost all of these genes play important roles in cellular and organismal-level processes other than aging, such as dauer formation, stress response, feeding, and chemosensation.

C. elegans之衰老过程涉及形态学、繁殖能力和行为学等方面的可测量下降。对导致该线虫衰老的细胞和分子机制的理解始于20世纪80年代初，当时通过针对性地鉴定延长寿命的突变体（即AGE表型）来启动研究。这些研究至少确定了两个寿命关键调节因子，DAF-2，一种胰岛素/IGF受体同源物，以及DAF-16，一种Forkhead相关转录因子。自那时起，许多更多参与衰老过程的基因和通路被识别出来。几乎所有这些基因在除衰老之外的其他细胞和生物体层面的过程中扮演着重要的角色，例如蛹形成、应激反应、摄食和化学感受等。