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. 2018 May 3;7:e32911. doi: 10.7554/eLife.32911

Figure 5. Bqt4 is required for resistance to agents that damage DNA during replication.

(A–C) Five-fold serial dilutions of log-phase cultures of the indicated strains were stamped onto media containing HU, MMS, or Bleomycin (see Materials and methods). To control for the effectiveness of Bleomycin, we used telomerase-deficient survivals that have circular chromosomes, previously shown to be bleomycin hypersensitive (Jain et al., 2010).

Figure 5.

Figure 5—figure supplement 1. The NE localization of Bqt4 is required for resistance to MMS, but not TBZ.

Figure 5—figure supplement 1.

(A) The transmembrane domain of Bqt4 (in the context of full length Bqt4) is required for resistance to MMS. Addition of GFP-Bqt4, but not GFP-Bqt4ΔTM, rescues the MMS sensitivity of bqt4Δ cells. Repeated rows indicate independent isolates of identical genotype. (B) bqt4Δ cells are not hypersensitive to the microtubule-destabilizing drug thiabendazole (TBZ). bqt4 deletion, however, does cause synthetic TBZ sensitivity with dcr1Δ. As expected (Reddy et al., 2011; Reyes-Turcu et al., 2011; Trewick et al., 2007), epe1 deletion rescues the growth defects and TBZ-hypersensitivity of dcr1Δ cells as well as dcr1Δbqt4Δ cells.