Figure 9.

Model for ATM-1 and ATL-1 functions during meiosis. We propose that ATM-1 is activated by DSBs and then promotes the timely resection of ends and repair using the homolog as a repair template. The excess RAD-51 foci in atm-1 mutants could be explained if ATM-1 inhibits DSBs (dotted line), perhaps through DSB-1, but possibly SPO-11 or other accessory factors. Alternatively, delayed resection and IH-CO formation could keep the feed-forward loop active longer to allow additional DSBs to be made. We further posit that ATL-1 is activated by resection intermediates, and both ATL-1 and a subset of pre-RAD-51 repair intermediates feed forward to promote additional DSB formation. ATL-1 then inhibits extensive resection and redundantly to ATM-1 helps to promote RAD-51 loading. These two activities can explain the delayed, excessive RAD-51 loading in atm-1;atl-1 double mutants.