Abstract：
:In nearly every organism studied, reduced caloric intake extends life span. In yeast, span extension from dietary restriction is thought to be mediated by the highly conserved, nutrient-responsive target of rapamycin (TOR), protein kinase A (PKA), and Sch9 kinases. These kinases coordinately regulate various cellular processes including stress responses, protein turnover, cell growth, and ribosome biogenesis. Here we show that a specific reduction of 60S ribosomal subunit levels slows aging in yeast. Deletion of genes encoding 60S subunit proteins or processing factors or treatment with a small molecule, which all inhibit 60S subunit biogenesis, are each sufficient to significantly increase replicative life span. One mechanism by which reduced 60S subunit levels leads to life span extension is through induction of Gcn4, a nutrient-responsive transcription factor. Genetic epistasis analyses suggest that dietary restriction, reduced 60S subunit abundance, and Gcn4 activation extend yeast life span by similar mechanisms.
journal_name
Celljournal_title
Cellauthors
Steffen KK,MacKay VL,Kerr EO,Tsuchiya M,Hu D,Fox LA,Dang N,Johnston ED,Oakes JA,Tchao BN,Pak DN,Fields S,Kennedy BK,Kaeberlein Mdoi
10.1016/j.cell.2008.02.037subject
Has Abstractpub_date
2008-04-18 00:00:00pages
292-302issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(08)00288-2journal_volume
133pub_type
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