Sinclair David A
Department of Pathology, Harvard Medical School, Boston MA 02115, USA.
Mech Ageing Dev. 2002 Apr 30;123(8):857-67. doi: 10.1016/s0047-6374(02)00023-4.
Over the past 10 years, considerable progress has been made in the yeast aging field. Multiple lines of evidence indicate that a cause of yeast aging stems from the inherent instability of repeated ribosomal DNA (rDNA). Over 16 yeast longevity genes have now been identified and the majority of these have been found to affect rDNA silencing or stability. Environmental conditions such as calorie restriction have been shown to modulate this mode of aging via Sir2, an NAD-dependent histone deacetylase (HDAC) that binds at the rDNA locus. Although this mechanism of aging appears to be yeast-specific, the longevity function of Sir2 is conserved in at least one multicellular organism, Caenorhabditis elegans (C. elegans). These findings are consistent with the idea that aging is a by-product of natural selection but longevity regulation is a highly adaptive trait. Characterizing this and other mechanisms of yeast aging should help identify additional components of longevity pathways in higher organisms.
在过去十年中,酵母衰老领域取得了显著进展。多条证据表明,酵母衰老的一个原因源于重复核糖体DNA(rDNA)固有的不稳定性。目前已鉴定出超过16个酵母长寿基因,其中大多数已被发现影响rDNA沉默或稳定性。诸如热量限制等环境条件已被证明可通过Sir2调节这种衰老模式,Sir2是一种依赖NAD的组蛋白脱乙酰酶(HDAC),它结合在rDNA位点。尽管这种衰老机制似乎是酵母特有的,但Sir2的长寿功能在至少一种多细胞生物秀丽隐杆线虫(C. elegans)中是保守的。这些发现与衰老为自然选择的副产物但长寿调节是高度适应性性状这一观点一致。表征酵母衰老的这一机制和其他机制应有助于识别高等生物中长寿途径的其他组成部分。