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. 2014 Dec 1;111(50):17827–17832. doi: 10.1073/pnas.1420096111

Fig. 5.

Fig. 5.

SWI/SNF–Sir3p interactions regulate resistance to replication stress and the establishment of telomeric silencing. (A) Growth assays. CEN/ARS plasmids containing SWI2 (CP1410), swi2–Δ10R (CP1413), or no insert (CP1250; pRS410) were introduced into swi2Δ or swi2Δ sir3Δ strains. WT and swi2–Δ10R complement swi2Δ growth and transcriptional defects, but swi2–Δ10R does not complement HU sensitivity. Fivefold serial dilutions of yeast cultures were spotted onto the indicated plates and allowed to grow for 3 d [yeast extract/peptone/dextrose (YPD)] or 6 d (all others) at 30 °C. (B, Left) Schematic of the subtelomeric silencing establishment assay. CY1755 (L1088; swi2Δ TELVR::URA3) was transformed with plasmids containing either SWI2 (CP1410) or swi2–Δ10R (CP1413), and transformant colonies were grown on SD–URA+G418 plates to select for Ura+ cells. Colonies were then cultured in medium lacking uracil for the indicated times and plated on 5-FOA plates to score establishment of silencing (Ura−). (Right) Representative 5-FOA plates after 24 h of growth on 5-FOA. (C) Quantitation of the assay from B. Five independent transformants were analyzed; error bars reflect SD.