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Department of Biochemistry and Biophysics, University of California San Francisco, San Francisco, California 94143-0448
Minichromosome maintenance (MCM) proteins are essential DNA replication factors conserved
among eukaryotes. MCMs cycle between chromatin
bound and dissociated states during each cell cycle. Their absence on chromatin is thought to contribute to
the inability of a G2 nucleus to replicate DNA. Passage
through mitosis restores the ability of MCMs to bind
chromatin and the ability to replicate DNA. In Drosophila early embryonic cell cycles, which lack a G1 phase,
MCMs reassociate with condensed chromosomes toward the end of mitosis. To explore the coupling between
mitosis and MCM-chromatin interaction, we tested
whether this reassociation requires mitotic degradation
of cyclins. Arrest of mitosis by induced expression of
nondegradable forms of cyclins A and/or B showed that
reassociation of MCMs to chromatin requires cyclin A
destruction but not cyclin B destruction. In contrast to
the earlier mitoses, mitosis 16 (M16) is followed by G1,
and MCMs do not reassociate with chromatin at the
end of M16. dacapo mutant embryos lack an inhibitor
of cyclin E, do not enter G1 quiescence after M16, and
show mitotic reassociation of MCM proteins. We propose that cyclin E, inhibited by Dacapo in M16, promotes chromosome binding of MCMs. We suggest that
cyclins have both positive and negative roles in controlling MCM-chromatin association.
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