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. 2017 Apr 7;18(6):1000–1012. doi: 10.15252/embr.201643560

Figure EV1. A synthetic viability screening identifies the SIR complex as the major driver of tof1∆ camptothecin hypersensitivity.

Figure EV1

  1. Spontaneous suppressors of camptothecin sensitivity of tof1∆ cells.
  2. Suppressor strains recovered from the tof1∆ synthetic viability screen are G418 resistant, suggesting presence of the TOF1 deletion cassette.
  3. Deletion of IRC15 does not suppress tof1∆ camptothecin hypersensitivity.
  4. Deletion of IME2 does not suppress tof1∆ camptothecin hypersensitivity.
  5. Deletion of SIR2 and deletion of TOP1 lead to similar levels of camptothecin resistance, and combining the two mutations does not further increase camptothecin resistance.
  6. Deletion of HML does not alter the camptothecin hypersensitivity of tof1∆ cells.
  7. tof1∆ cells and congenic wild‐type cells were pre‐grown either in the absence or in the presence of sirtinol. They were subsequently synchronised in G1 and released into S phase in the presence of camptothecin, either with or without sirtinol. Cell cycle progression was monitored by FACS analysis.