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.