Models for role of TRIP13^PCH-2 in spindle checkpoint activation. Two models for how TRIP13^PCH-2 regulates spindle checkpoint activation discussed in the text are depicted. During checkpoint activation, the Mad1/C-Mad2 complex is recruited to unattached kinetochores. In model 1, TRIP13^PCH-2 removes an inhibitory p31(comet)^CMT-1 “cap” from kinetochore bound Mad1/C-Mad2 to allow free O-Mad2 to dimerize with C-Mad2 at the kinetochore, converting it to C-Mad2, promoting MCC formation and preventing anaphase. In model 2, TRIP13^PCH-2 localizes to kinetochores where it interacts with p31(comet)^CMT-1/C-Mad2, releasing O-Mad2 from p31(comet)^CMT-1. This allows for O-Mad2 to dimerize with Mad1/C-Mad2 at the kinetochore, promoting the generation of additional soluble C-Mad2, MCC production, and an anaphase delay.