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  • Title: Mad1 contribution to spindle assembly checkpoint signalling goes beyond presenting Mad2 at kinetochores.
    Author: Heinrich S, Sewart K, Windecker H, Langegger M, Schmidt N, Hustedt N, Hauf S.
    Journal: EMBO Rep; 2014 Mar; 15(3):291-8. PubMed ID: 24477934.
    Abstract:
    The spindle assembly checkpoint inhibits anaphase until all chromosomes have become attached to the mitotic spindle. A complex between the checkpoint proteins Mad1 and Mad2 provides a platform for Mad2:Mad2 dimerization at unattached kinetochores, which enables Mad2 to delay anaphase. Here, we show that mutations in Bub1 and within the Mad1 C-terminal domain impair the kinetochore localization of Mad1:Mad2 and abrogate checkpoint activity. Artificial kinetochore recruitment of Mad1 in these mutants co-recruits Mad2; however, the checkpoint remains non-functional. We identify specific mutations within the C-terminal head of Mad1 that impair checkpoint activity without affecting the kinetochore localization of Bub1, Mad1 or Mad2. Hence, Mad1 potentially in conjunction with Bub1 has a crucial role in checkpoint signalling in addition to presenting Mad2.
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