Mutual Antagonism Between the Anaphase Promoting Complex and the Spindle Assembly Checkpoint Contributes to Mitotic Timing in Caenorhabditis elegans
Author(s) -
Alexandra Bezler,
Pierre Gönczy
Publication year - 2010
Publication title -
genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.792
H-Index - 246
eISSN - 1943-2631
pISSN - 0016-6731
DOI - 10.1534/genetics.110.123133
Subject(s) - biology , spindle checkpoint , microbiology and biotechnology , anaphase , mad2 , spindle apparatus , mitosis , caenorhabditis elegans , sister chromatids , cohesin , mitotic exit , genetics , anaphase promoting complex , cell cycle , cell division , meiosis , cell , chromosome , gene
The anaphase promoting complex/cyclosome (APC/C) triggers the separation of sister chromatids and exit from mitosis across eukaryotic evolution. The APC/C is inhibited by the spindle assembly checkpoint (SAC) until all chromosomes have achieved bipolar attachment, but whether the APC/C reciprocally regulates the SAC is less understood. Here, we report the characterization of a novel allele of the APC5 component SUCH-1 in Caenorhabditis elegans. We find that some such-1(t1668) embryos lack paternally contributed DNA and centrioles and assemble a monopolar spindle in the one-cell stage. Importantly, we show that mitosis is drastically prolonged in these embryos, as well as in embryos that are otherwise compromised for APC/C function and assemble a monopolar spindle. This increased duration of mitosis is dependent on the SAC, since inactivation of the SAC components MDF-1/MAD1 or MDF-2/MAD2 rescues proper timing in these embryos. Moreover, partial depletion of the E1 enzyme uba-1 significantly increases mitosis duration upon monopolar spindle assembly. Taken together, our findings raise the possibility that the APC/C negatively regulates the SAC and, therefore, that the SAC and the APC/C have a mutual antagonistic relationship in C. elegans embryos.
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