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. 2014 Jan 14;196(4):985–999. doi: 10.1534/genetics.113.158295

Figure 6.

Figure 6

BRC-1/BRD-1 promote genome instability when SMC-5/6 dysfunction leads to replication stalling and aberrant HR. (A) αRAD-51 and DAPI staining of mitotic germ cells. Young adults were dissected 5 hr after either UVB irradiation or mock treatment. Representative images are shown. Bar, 10 µm. (B) αBRD-1 and DAPI staining of mitotic germ cells. Germlines were dissected from young adult worms. Representative images in extended view of stack spanning the whole germline are shown. Bar, 10 µm. (C) Model for DNA repair mechanisms in the presence and absence of SMC-5/6. In proliferating wild-type cells, SMC-5/6 prevents fork stalling. Upon stalling, TLS promotes readthrough, while the BRC-1/BRD-1 complex initiates HR and SMC-5/6 promotes dissociation of BRC-1/BRD-1 from chromatin. Defective SMC-5/6 sensitizes to replication stalling, and TLS becomes the major route for replication fork restart, while BRC-1/BRD-1 initiate HR that, however, cannot be resolved in the absence of SMC-5/6 but instead leads to persistence of HR intermediates. In the absence of BRC-1/BRD-1, the formation of HR intermediates is prevented and TLS can promote lesion bypass.