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. 2004 Dec 23;24(2):405–417. doi: 10.1038/sj.emboj.7600511

Figure 7.

Figure 7

Different pathways use the RecQ helicase in response to replication stalling. Stalled replication forks activate Rad53p kinase in the absence of strand breaks in an Sgs1p-, Mrc1- and Mec1-dependent pathway that is independent of Top3p and Rad51p. Forks are stabilised by two mechanisms, including one that requires Rad51p and the Sgs1p/Top3p complex. We proposed that the Rad51p-dependent pathway leads to the formation of a four-way DNA junction due to fork reversal. DSBs will form at some of the stalled replication forks, and will activate the intra-S damage pathway (breakage pathway) for checkpoint activation, which relies on Rad24p and the 9-1-1 complex.

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