Journal
JOURNAL OF CELL SCIENCE
Volume 129, Issue 13, Pages 2493-2499Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/jcs.189910
Keywords
Meiosis; Wave; Gonad; Germ cell; Migration; Ror2
Categories
Funding
- California Institute for Regenerative Medicine [TG TG2-01153]
- National Institutes of Health [TG 5T32HD007263-32, DP2OD007420 S1, 1R21ES023297, DP2OD007420]
- Irtelis (Commissariat a l'Energie Atomique et aux Energies Alternatives)
- Fondation ARC pour la Recherche sur le Cancer
- National Science Foundation fellowship
- University of California
- San Francisco Program for Breakthrough Biomedical Research
- Institut Universitaire de France
- generous philanthropy
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Mouse ovarian germ cells enter meiosis in a wave that propagates from anterior to posterior, but little is known about contribution of germ cells to initiation or propagation of meiosis. In a Ror2 mutant with diminished germ cell number and migration, we find that overall timing of meiotic initiation is delayed at the population level. We use chemotherapeutic depletion to exclude a profoundly reduced number of germ cells as a cause for meiotic delay. We rule out sex reversal or failure to specify somatic support cells as contributors to the meiotic phenotype. Instead, we find that anomalies in the distribution of germ cells as well as gonad shape in mutants contribute to aberrant initiation of meiosis. Our analysis supports a model of meiotic initiation via diffusible signal(s), excludes a role for germ cells in commencing the meiotic wave and furnishes the first phenotypic demonstration of the wave of meiotic entry. Finally, our studies underscore the importance of considering germ cell migration defects while studying meiosis to discern secondary effects resulting from positioning versus primary meiotic entry phenotypes.
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