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Vol. 11, Issue 4, 1401-1419, April 2000
¶
*Department of Cell Biology, Vanderbilt University School of
Medicine, Nashville, Tennessee 37232; Here we show that emb-30 is required for
metaphase-to-anaphase transitions during meiosis and mitosis in
Caenorhabditis elegans. Germline-specific
emb-30 mutant alleles block the meiotic divisions. Mutant oocytes, fertilized by wild-type sperm, set up a meiotic spindle
but do not progress to anaphase I. As a result, polar bodies are not
produced, pronuclei fail to form, and cytokinesis does not occur.
Severe-reduction-of-function emb-30 alleles (class I
alleles) result in zygotic sterility and lead to germline and somatic
defects that are consistent with an essential role in promoting the
metaphase-to-anaphase transition during mitosis. Analysis of the vulval
cell lineages in these emb-30(class I) mutant animals
suggests that mitosis is lengthened and eventually arrested when
maternally contributed emb-30 becomes limiting. By
further reducing maternal emb-30 function contributed to
class I mutant animals, we show that emb-30 is required
for the metaphase-to-anaphase transition in many, if not all, cells.
Metaphase arrest in emb-30 mutants is not due to
activation of the spindle assembly checkpoint but rather reflects an
essential emb-30 requirement for M-phase progression. A
reduction in emb-30 activity can suppress the lethality and sterility caused by a null mutation in mdf-1, a
component of the spindle assembly checkpoint machinery. This result
suggests that delaying anaphase onset can bypass the spindle checkpoint requirement for normal development. Positional cloning established that
emb-30 encodes the likely C. elegans
orthologue of APC4/Lid1, a component of the anaphase-promoting
complex/cyclosome, required for the metaphase-to-anaphase transition.
Thus, the anaphase-promoting complex/cyclosome is likely to be required
for all metaphase-to-anaphase transitions in a multicellular organism.
Umeå Center for
Molecular Pathogenesis, Umeå University, Umeå, Sweden;
§Department of Medical Genetics, University of British
Columbia, Vancouver, British Columbia, V6T 1Z3 Canada; and
The E. Bronson Ingram Cancer Center, Vanderbilt
University, Nashville, Tennessee 37232
Present address: Department of Pathology,
Harvard Medical School, Boston, MA 02115.
¶
Corresponding author. E-mail address:
david.greenstein{at}mcmail.vanderbilt.edu.
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