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RESEARCH COMMUNICATION

Germ cell aneuploidy in zebrafish with mutations in the mitotic checkpoint gene mps1

¹ Howard Hughes Medical Institute, ² Department of Cell Biology and ³ Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115, USA; ⁴ Department of Cardiology and ⁵ Department of Pathology, Children's Hospital, Boston, Massachusetts 02115, USA; ⁶ Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA; ⁷ Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710, USA

Aneuploidy, resulting from chromosome missegregation during meiosis, is a major cause of human infertility and birth defects. However, its molecular basis remains incompletely understood. Here we have identified a spectrum of chromosome anomalies in embryos of zebrafish homozygous for a hypomorphic mutation in Mps1, a kinase required for the mitotic checkpoint. These aneuploidies are caused by meiotic error and result in severe developmental defects. Our results reveal Mps1 as a critical regulator of chromosome number in zebrafish, and demonstrate how slight genetic perturbation of a mitotic checkpoint factor can dramatically reduce the fidelity of chromosome segregation during vertebrate meiosis.

[Keywords: Zebrafish; aneuploidy; meiosis; spindle checkpoint; Mps1; nondisjunction]

Received December 30, 2003; revised version accepted May 11, 2004.

¹⁰ Corresponding author. E-MAIL k.poss{at}cellbio.duke.edu; FAX (919) 684-5481.

⁸ Present address: Department of Biological Structure, University of Washington, Seattle, WA 98195, USA

⁹ Present address: Department of Pathology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

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