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. 2010 Jan 19;107(12):5522–5527. doi: 10.1073/pnas.0909169107

Fig. 2.

Fig. 2.

The synthetic lethality between the Rpd3(L) and the SAS-I complex is caused by inappropriate SIR spreading. (A) Deletions of subunits of the telomeric SIR complex suppress the sas2Δ rpd3Δ synthetic lethality. Derivatives of an sas2Δ rpd3Δ pURA3-SAS2 strain (AEY 3923) with deletions for SIR1, SIR2, SIR3, or SIR4 were grown on minimal plates (YM, growth assay) and on 5-FOA plates to select against pURA3-SAS2 for 2 days at 30°C. (B) Mutations within the histone H3 and H4 N-termini suppress the sas2Δ rpd3Δ synthetic lethality. Alleles of H3 and H4 were introduced into an rpd3Δ sas2Δ pLYS2-SAS2 strain by plasmid shuffle (AEY3945; SI Materials and Methods for details), and the ability of the derivatives to survive in the absence of the SAS2 plasmid was tested. “wt” refers to WT copies of H3 and H4 in AEY3945. “Control” refers to a WT strain. H4 K -> Q designates H4 K5, 8, 12, and 16 Q. H3 K -> Q designates H3 K4, 9, 14, 18, 23, and 27 Q.