Figure 7.

Summary of kinetochore and PKA interactions. At a restrictive temperature, the ndc10-1 mutant does not assemble a kinetochore; therefore, microtubules cannot attach and Mad2 cannot be recruited. The ipl1-321 mutant has functional kinetochores that attach to the same pole, but Mad2 is not recruited (Gillett et al. 2004). The spc24-8 mutant is checkpoint active; therefore, Mad2 is presumed to be properly localized to the kinetochore. The spc24-8 mad2Δ mutant lacks Mad2 and is spindle checkpoint defective; however, kinetochores are still present. The state of the kinetochore-microtubule interaction in spc24-8 mad2Δ cells has not been investigated. The kinetochores in spc24-9 and spc24-10 mutants have defects in microtubule attachment and are presumed to mislocalize Mad2 as the spindle elongates in both mutants, despite attachment defects. In addition, similar mutants in the Ndc80 complex mislocalize Mad2 (Gillett et al. 2004). Genetic interactions upon overexpression of BCY1 or PDE2, deletion of RAS2 (ras2Δ), or expression of RAS2^val19 in each kinetochore mutant is represented with a plus (+) sign if growth defects were improved and minus (−) sign if growth defects were exacerbated.