Figure 8.—

Model of the relationship between SC and DNA damage checkpoints. Proteins and events involved in normal cell cycle progression are indicated in black; proteins and events involved in checkpoint-induced cell cycle arrest are depicted in red. Pch2 might function to ensure proper coupling between SC morphogenesis and meiotic recombination. A signal from aberrant SC could signal Pch2 to inhibit late steps in recombination, either by preventing the completion of recombination or by blocking progression to the stage in the cell cycle when recombination normally is completed. Accumulation of recombination intermediates would then trigger the DNA damage checkpoint, dependent on Ddc1/Mec3/Rad17. Wu and Burgess (2006) have shown that almost all of the spores produced by a pch2 rad17 double mutant are inviable, suggesting that Pch2 and/or Rad17 have additional unknown functions.