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. Author manuscript; available in PMC: 2014 Mar 26.
Published in final edited form as: Mol Cell. 2010 Sep 10;39(5):724–735. doi: 10.1016/j.molcel.2010.08.015

Figure 2. Genetic identification of the pathway through which Asf1 regulates replicative lifespan.

Figure 2

A. Replicative aging analysis of wild type W303 yeast (“WT”) or this strain deleted for ASF1 (“asf1”), CAC1 (“cac1”) or both ASF1 and CAC1 (“asf1cac1”). B. Isogenic strains that were wild type (BY4741) or deleted for ASF1 or MRC1 from the genome wide deletion collection in the S288c strain background were analyzed for replicative lifespan. C. Replicative aging analysis of yeast strains YB (“WT”), ZGY608 (“asf1”), ZGY906 (“rtt109”), and ZGY964 (“asf1rtt109”). D. Replicative aging analysis of yeast strains HMY152 (“WT”), JFY004 (“asf1”), HMY139 (“H3 K56Q”), HMY140 (“H3 K56R”), JFY005 (“H3 K56Q asf1”), and JFY006 (“H3 K56R asf1”). E. Replicative aging analysis of isogenic yeast strains BY4741 (“WT”) and YNML7 (“hst3hst4”). F. Replicative aging analysis of isogenic yeast strains SHY0015 (“WT”) and SHY0014 (“pGALAsf1”). 0.5% galactose leads to endogenous levels of Asf1, while 1% galactose leads to higher than endogenous levels of Asf1 (Zabaronick and Tyler, 2005).