Sic1 plays a strong role in Far1-independent arrest. PGAL1-CDC20 strains of the indicated genotypes were synchronized and then released into the presence or absence of α factor (αF). Cell cycle progression and G1 arrest was assayed by budding. (A, B) Results in the FAR1 cln2∆ and far1∆ cln2∆ backgrounds, respectively. All graphs show the mean ± SD (n = 4–6). Note that far1∆ cln2∆ cdh1∆ strains showed phenotypic heterogeneity that was isolate dependent. Specifically, we tested 12 isolates: six PGAL1-CDC20 derivatives from each of two independent far1∆ cln2∆ cdh1∆ strains. The results shown are an average of three strains (YPAP242, 244, 245) that displayed the majority phenotype seen in 10 of 12 isolates. In two of 12 isolates, both derived from the same initial far1∆ cln2∆ cdh1∆ parent strain, we observed a notable escape phenotype (e.g., for YPAP243, ∼40% budded cells after 120–180 min in α factor). The reason for this heterogeneity is unknown, but the observation of the escape phenotype in only a minority of derivatives (2/6) of one parent strain and in no derivatives (0/6) of the other suggests that a rare enhancer mutation may be responsible.