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. 2005 Nov;171(3):885–899. doi: 10.1534/genetics.105.044719

Figure 2.

Figure 2.

Mec1 and Rad53 have opposing roles in regulating the strength of telomeric silencing. Log-phase cultures of the indicated genotypes were plated onto rich media (YPD) or synthetic media containing 5′-FOA. All strains contained URA3-VIIL (Gottschling et al. 1990). (A) Deletion of SML1 has no effect on telomeric silencing. Strains were PKY090 (wild type), PKY638 (cac1Δ), PKY1766 (sml1Δ), and PKY1769 (cac1Δ sml1Δ). (B) Synergistic loss of telomeric silencing in cac1Δ mec1Δ double-mutant cells. Strains were PKY1766 (sml1Δ), PKY1769 (cac1Δ sml1Δ), PKY1768 (mec1Δ sml1Δ), and PKY1771 (cac1Δ mec1Δ sml1Δ). (C) Deletion of RAD53 suppresses the telomeric silencing defect in cac1Δ cells. Strains were PKY2704 (sml1Δ), PKY2706 (cac1Δ sml1Δ), PKY2702 (rad53Δ sml1Δ), and PKY2710 (cac1Δ rad53Δ sml1Δ). (D) Deletion of PDS1 has no effect on telomeric silencing. Strains were PKY090 (wild type), PKY638 (cac1Δ), PKY3611 (pds1Δ), and PKY3616 (cac1Δ pds1Δ).