Fig. 5: The BRCA2–MCM10 association restrains replication fork progression after DNA damage. | Nature Communications

Fig. 5: The BRCA2–MCM10 association restrains replication fork progression after DNA damage.

From: BRCA2 associates with MCM10 to suppress PRIMPOL-mediated repriming and single-stranded gap formation after DNA damage

Fig. 5

a Schematic diagram of MCM10 domain structure and amino acid sequence alignment of the MCM10 N-terminal coiled-coil (CC) motif. b Co-IP of endogenous BRCA2 with FLAG-HA-tagged MCM10 proteins transiently overexpressed in 293T cells. c Expression levels and association between exogenous MCM10 proteins and endogenous BRCA2 in U2OS cell lines stably expressing FLAG-HA-tagged WT and CC mutant MCM10 proteins. For (b) and (c), similar results were obtained in n = 3 independent experiments. df Replication tract lengths in U2OS cells selectively expressing exogenous WT or mutant MCM10 proteins before or 6 h after 10 Gy of IR (d), 3 h after 2 Gy of IR (e), or after 6 h of continuous treatment with DMSO (vehicle) or 1 µM BLEO (f). g Replication tract lengths in the above cells before and after IR as determined by the DNA combing assay. A representative combing image is shown on the left. h Stability of stalled replication forks in the above cells. Assay scheme is shown on the top, and IdU/CldU tract length ratio after HU treatment is shown below. Data in (dh) are presented as mean ± s.d., with the number of dots shown below each column. P values are determined two-tailed unpaired Student’s t test. Similar results were obtained from n = 2 independent experiments. Source data are provided as a Source Data file.

Back to article page