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. Author manuscript; available in PMC: 2022 Jul 15.
Published in final edited form as: Mol Cell. 2021 Jun 8;81(14):3007–3017.e5. doi: 10.1016/j.molcel.2021.05.014

Figure 6. A direct interaction of RADX and RAD51 is required to maintain fork stability in cells experiencing persistent replication stress.

Figure 6.

(A) Fork protection assays with 3mM HU were performed in U2OS cells immediately after infection with lentiviruses to overexpress wild-type (WT) RADX or RADX QVPK. Arrows in the immunoblot indicate the endogenous and GFP-tagged RADX proteins. (B) Wild-type or RADXΔ U2OS cells complemented with WT RADX or RADX QVPK were transfected with non-targeting or BRCA2 siRNA and examined for fork protection. Note that the wild-type RADX but not the RADX QVPK mutant expression in the RADXΔ complemented cells decreases after a few passages as previously reported (Adolph et al., 2021). A one-way ANOVA with Tukey’s multiple comparison test was used to calculate all p values. All experiments were completed at least three times. Extra lanes were removed.