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First published online March 30, 2004
doi: 10.1242/10.1242/dev.01054

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Inhibition of the cell cycle is required for convergent extension of the paraxial mesoderm during Xenopus neurulation

Walter F. Leise, III^1,* and Paul R. Mueller^2,

¹ Department of Biochemistry and Molecular Biology, University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA
² Department of Molecular Genetics and Cell Biology, Center for Molecular Oncology, and Committees on Developmental Biology, Cancer Biology, and Genetics, University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA

Author for correspondence (e-mail: pmueller{at}midway.uchicago.edu)

Accepted 22 December 2003

Coordination of morphogenesis and cell proliferation is essential during development. In Xenopus, cell divisions are rapid and synchronous early in development but then slow and become spatially restricted during gastrulation and neurulation. One tissue that transiently stops dividing is the paraxial mesoderm, a dynamically mobile tissue that forms the somites and body musculature of the embryo. We have found that cessation of cell proliferation is required for the proper positioning and segmentation of the paraxial mesoderm as well as the complete elongation of the Xenopus embryo. Instrumental in this cell cycle arrest is Wee2, a Cdk inhibitory kinase that is expressed in the paraxial mesoderm from mid-gastrula stages onwards. Morpholino-mediated depletion of Wee2 increases the mitotic index of the paraxial mesoderm and this results in the failure of convergent extension and somitogenesis in this tissue. Similar defects are observed if the cell cycle is inappropriately advanced by other mechanisms. Thus, the low mitotic index of the paraxial mesoderm plays an essential function in the integrated cell movements and patterning of this tissue.

Key words: Xenopus, Wee1, Wee2, Cdk, Cell cycle, Morphogenesis, Convergent extension, Somitogenesis

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