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. 2013 Nov 20;8(11):e81015. doi: 10.1371/journal.pone.0081015

Figure 5. The Rad53 checkpoint function of Rad9 is not required for GCR suppression and growth in the presence of MMS in cells lacking Sgs1.

Figure 5

(A) Illustration of the domain structure of Rad9. (B) Immunoprecipitations were conducted with extracts from the contructed rad9 7xA-HA strain (LBy-471) and the sgs1Δrad9 7xA-HA strain (LBy-472) to verify the 7xA mutations. Immunoprecipitations were performed with anti-HA antibody in the presence and absence of MMS. (C) Survival was monitored as described in Materials and Methods after 70 min exposure to different concentrations of MMS for the indicated strains: wild type (LBy-1), sgs1Δ (LBy-129), rad9Δ (LBy-316), sgs1Δrad9Δ (LBy-44), rad9 7xA (LBy-471), sgs1Δ rad9 7xA (LBy-472). (D) GCR were measured after exposure to 0.02% MMS and is shown as fold increase over wild type for the isogenic strains: sgs1Δ (LBy-388), rad24Δ (LBy-406), rad9Δ (LBy-389), rad9 7xA (LBy-473), sgs1Δ rad9 7xA (LBy-474).