Deletion of SGS1 causes premature aging including a shortened replicative lifespan by approximately 60%, sterility, fragmentation of the nucleolus and redistribution of the Sir3 silencing protein from telomeres to the nucleolus [Sinclair et al, 1997]. Mutation in SGS1 shortens replicative lifespan by 30% [11290710]. Introduction of mutant allele with a point mutation (SGS1 K(706)-->A) in the RecQ helicase domain that eliminates the DNA helicase activity of Sgs1 fails to rescue the premature aging of the sgs1Delta strain, demonstrating that Sgs1 DNA helicase activity is required for a normal lifespan [11861900].

Most cell death in sgs1 mutant cells is caused by a stochastic cell cycle arrest that is associated with a large-budded terminal morpholgy [McVey et al, 2001]. Overexpression of SIR2 or deletion of FOB1 extend lifespan of only those sgs1 cells that escape this arrest [11290710; 10230397].

Overexpression of SGS1 extends the maximum lifespan of cells lacking SRS2, but not the mean lifespan [11861900].

sgs1 mutants have greater rate of telomere loss than wild-type cells in the abscence of telomerase [11179234].

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