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. Author manuscript; available in PMC: 2013 Sep 20.
Published in final edited form as: DNA Repair (Amst). 2011 Oct 28;11(2):131–138. doi: 10.1016/j.dnarep.2011.10.012

Fig. 4. RAD18-BRCTx interaction is required for efficient repair of UV-induced DNA damage.

Fig. 4

(A) The S442/444A mutant of RAD18 is defective in restoring cell survival after UV treatment. RAD18-deficient cells were transduced with a control virus or a virus expressing HA-Flag-tagged wild-type RAD18 or the serine double mutant (S442/444A), which does not bind to BRCTx. Cell survival assays were performed as described in Materials and Methods. Date are presented as means and SD (error bars) from three independent experiments. (B) Binding to BRCTx is not required for RAD18 function in UV-induced PCNA monoubiquitination. RAD18-deficient cells were transduced with a control virus or a virus expressing HA-Flag-tagged wild-type RAD18 or the serine double mutant (S442/444A), which does not bind to BRCTx. Chromatin fractions were isolated (see Materials and Methods) and immunoblotted with the indicated antibodies. (C) Binding to BRCTx is not required for RAD18 function in homologous recombination. Gene conversion assays were performed as described in Materials and Methods. The percentage of GFP-positive cells was determined by flow cytometry 48 h after electroporation. Data shown are Means and SD (error bars) from three independent experiments.