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. Author manuscript; available in PMC: 2008 Oct 12.
Published in final edited form as: Mol Cell. 2007 Oct 12;28(1):134–146. doi: 10.1016/j.molcel.2007.09.009

Figure 3. Exo1 Can Substitute for Ctp1 in Repair of DSBs and Recruitment of RPA to a DSB is Defective in ctp1Δ Cells.

Figure 3

(A) The IR and CPT survival defects of ctp1Δ cells are suppressed by eliminating Ku80. This rescue depends on Exo1.

(B) Recruitment of RPA to a DSB is reduced in ctp1Δ and mre11Δ strains relative to wild type. ChIP analysis of RPA (rad11-TAP) around an HO-induced DSB. Expression of HO endonuclease was controlled using the thiamine-repressible nmt1 promoter. Sites located 0.2, 2, 9 and 16 kb from the DSB were assayed for enrichment of RPA (see Figure 4 for map of probes). The act1 probe is included as a negative control. Microscopic analyses confirmed that >90% of the cells in all strains arrested division as a result of HO expression, confirming highly efficient cutting by HO endonuclease.

(C) Recruitment of RPA to a DSB is reduced in ctp1Δ and mre11Δ strains relative to wild type. Quantitative real-time PCR was used to measure enrichment of RPA at sites located 0.2 or 9 kb from the HO-induced DSB.