Fig. 5. Deletion of Sis1 G/F or CTD regions eliminates the hybrid [RPS⁺] prion and [RNQ⁺] in 74D-694 cells. The presence of [RPS⁺] allows survival on media lacking adenine and growth into white colonies on YPD because of the epigenetic inactivation of the Sup35 C-terminal region. Sis1-replacement derivatives from a 74D-694 [RPS⁺] background were created as described above. These were plated by 5-fold serial dilution to YPD and SD-ade (A). Yeast deleted for the CTD or both the G/M region and the CTD of Sis1 had a notable slow-growth phenotype at 30°C. These colonies were red on YPD and showed no apparent growth on SD-ade within a week. Strains deleted for G/F had a wild-type growth rate on YPD, but also lost the ability to grow on SD-ade. To investigate the possibility that Sis1 plays a strain-specific role in prion maintenance in 74D-694, we examined the effect of the Sis1 deletion proteins on [RNQ⁺] maintenance in these strains by centrifugation assay (B). All tested SIS1 deletions led to a loss of [RNQ⁺].