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The DNA damage checkpoint kinase Mec1(ATR) is critical for maintaining the integrity of replication forks. Mec1 mediates a key interaction between the fork protein Dpb11 and the DNA repair scaffolds Slx4-Rtt107 to regulate replication stress response. Dissection of the molecular basis of the interaction reveals that Slx4 and Rtt107 jointly bind Dpb11 and that Slx4 phosphorylation is required. Multiple fork repair factors associate with Rtt107 or Slx4, supporting that Mec1-dependent assembly of the Rtt107-Slx4-Dpb11 complex functions to coordinate fork repair.
DNA damage signaling recruits the Rtt107-Slx4 scaffolds via Dpb11 (Mec1-dependent assembly of the Rtt107-Slx4-Dpb11 complex) to mediate replication stress response.
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