The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms
The SIR2/3/4 complex and SIR2 alone promote longevity in Saccharomyces cerevisiae by two different mechanisms
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DOI：
10.1101/gad.13.19.2570
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发表时间：
1999-10-01
影响因子：
10.5
通讯作者：
Guarente, L
中科院分区：
文献类型：
--
作者：
Kaeberlein, M;McVey, M;Guarente, L
SIR基因是酵母母细胞寿命的决定因素。在这里，我们表明，由爵士蛋白质的生活剥落调节是独立的非同源末端连接中的作用。sir3或sir4突变体的短寿命是由于α和α交配型信息的同时表达，这间接导致rDNA重组的增加，并可能增加染色体外rDNA环的产生。sir2突变体的短寿命也揭示了抑制由rDNA中Fob1p介导的复制阻断产生的重组的直接失败。Sir2p是促进酵母寿命的限制性成分，增加基因剂量可以延长野生型细胞的寿命。保守的SIR2在哺乳动物衰老中的可能作用进行了讨论。
The SIR genes are determinants of life span in yeast mother cells. Here we show that life spall regulation by the Sir proteins is independent of their role in nonhomologous end joining. The short life span of a sir3 or sir4 mutant is due to the simultaneous expression of a and alpha mating-type information, which indirectly causes an increase in rDNA recombination and likely increases the production of extrachromosomal rDNA circles. The short life span of a sir2 mutant also reveals a direct failure to repress recombination generated by the Fob1p-mediated replication block in the rDNA. Sir2p is a limiting component in promoting yeast longevity, and increasing the gene dosage extends the life span in wild-type cells. A possible role of the conserved SIR2 in mammalian aging is discussed.