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. 2012 Aug;191(4):1107–1118. doi: 10.1534/genetics.112.141713

Figure 2 .

Figure 2 

Inactivation or overexpression of HSP104 rescues rkr1Δ synthetic genetic interactions. (A) Heterozygous rtf1Δ/RTF1 rkr1Δ/RKR1 diploids (KY2202 mated by KY453) were dissected onto YPD or YPD containing 2.5 mM GuHCl and incubated at 30° for 3 days. (B) An rtf1Δ rkr1Δ [RTF1/URA3] strain (KY1663) was transformed with either a 2µ TRP1-marked pGPD-HSP104 plasmid or a TRP1-marked empty vector (pRS424), and transformants were purified on SC-W and replica-plated to SC-W + 5-FOA (W = tryptophan). Plates were incubated at 30° for 3 days. (C) Wild-type (KY2203) or rkr1Δ (KY2204) strains, lacking both endogenous histone H2A and H2B gene copies and containing a URA3-marked wild-type copy of HTA1-HTB1, were transformed with a HIS3-marked HTA1-htb1 K123R plasmid. Strains were cured by streaking onto YPD + 5 mM GuHCl. Dilution growth assays were performed on SC-H or SC-H + 5-FOA, and cells were incubated at 30° for 2 days (H = histidine). “PRION+” indicates uncured cells; “prion−” indicates cells passaged on medium containing GuHCl.