Wasko Brian M, Kaeberlein Matt
Department of Pathology, University of Washington, Seattle, WA, USA.
FEMS Yeast Res. 2014 Feb;14(1):148-59. doi: 10.1111/1567-1364.12104. Epub 2013 Oct 30.
The finite replicative life span of budding yeast mother cells was demonstrated as early as 1959, but the idea that budding yeast could be used to model aging of multicellular eukaryotes did not enter the scientific mainstream until relatively recently. Despite continued skepticism by some, there are now abundant data that several interventions capable of extending yeast replicative life span have a similar effect in multicellular eukaryotes including nematode worms, fruit flies, and rodents. In particular, dietary restriction, mTOR signaling, and sirtuins are among the most studied longevity interventions in the field. Here, we describe key conserved longevity pathways in yeast and discuss relationships that may help explain how such broad conservation of aging processes could have evolved.
早在1959年就已证明出芽酵母母细胞的有限复制寿命,但直到最近,利用出芽酵母来模拟多细胞真核生物衰老的想法才进入科学主流。尽管仍有一些人持怀疑态度,但现在有大量数据表明,几种能够延长酵母复制寿命的干预措施在包括线虫、果蝇和啮齿动物在内的多细胞真核生物中具有类似作用。特别是,饮食限制、mTOR信号传导和去乙酰化酶是该领域研究最多的长寿干预措施。在这里,我们描述了酵母中关键的保守长寿途径,并讨论了一些关系,这些关系可能有助于解释衰老过程的如此广泛保守是如何进化而来的。