CUL-2 and ZYG-11 promote meiotic anaphase II and the proper placement of the anterior-posterior axis in C. elegans.
2004
The faithful segregation of chromosomes during meiosis is vital for sexual
reproduction. Currently, little is known about the molecular mechanisms
regulating the initiation and completion of meiotic anaphase. We show that
inactivation of CUL-2, a member of the cullin family of ubiquitin ligases,
delays or abolishes meiotic anaphase II with no effect on anaphase I,
indicating differential regulation during the two meiotic stages. In
cul-2 mutants, the cohesin REC-8 is removed from chromosomes normally
during meiosis II and sister chromatids separate, suggesting that the failure
to complete anaphase results from a defect in chromosome movement rather than
from a failure to sever chromosome attachments. CUL-2 is required for the
degradation of cyclin B1 in meiosis and inactivation of cyclin B1 partially
rescued the meiotic delay in cul-2 mutants. In cul-2
mutants, the failure to degrade cyclin B1 precedes the metaphase II arrest.
CUL-2 is also required for at least two aspects of embryonic polarity. The
extended meiosis II in cul-2 mutants induces polarity reversals that
include reversed orientation of polarity proteins, P granules, pronuclei
migration and asymmetric cell division. Independently of its role in meiotic
progression, CUL-2 is required to limit the initiation/spread of the polarity
protein PAR-2 in regions distant from microtubule organizing centers. Finally,
we show that inactivation of the leucine-rich repeat protein ZYG-11 produces
meiotic and polarity reversal defects similar to those observed in
cul-2 mutants, suggesting that the two proteins function in the same
pathways.
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