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. 2011 Sep 22;7(9):e1002291. doi: 10.1371/journal.pgen.1002291

Figure 12. Potential mechanisms to produce SCE (panel A), chromatid breaks (panel B), and SCU (panel C) upon replication fork blockage.

Figure 12

BCCIP may function to promote the Rad51-dependent strand invasion (thus SCE) and reduce the probability of further collapse of replication forks to form the 3-ended DNA double strand break ends (panel C) that would lead to the formation of SCU, or permanently form the one-ended DSB structures (panel B) that lead to the formation of single chromatid breaks (see text for more details).