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. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: Mol Microbiol. 2011 Jun 28;81(2):515–527. doi: 10.1111/j.1365-2958.2011.07714.x

Fig. 8.

Fig. 8

Proposed model for Sit4p-dependent oxidative stress sensitivity and shortened chronological lifespan of isc1Δ cells. Cells lacking Isc1p display an increase in dh-C26-Cer and phyto-C26-Cer species, probably due to de novo biosynthesis, that activate Sit4p. Dephosphorylation of Sit4p target proteins causes mitochondrial dysfunction, leading to oxidative stress sensitivity and shortened chronological lifespan in isc1Δ cells. SIT4 deletion restores mitochondrial function of isc1Δ cells, increasing oxidative stress resistance and chronological lifespan.