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First published online 13 August 2008
doi: 10.1242/dev.022897

Development 135, 3053-3062 (2008)
Published by The Company of Biologists 2008
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Chato, a KRAB zinc-finger protein, regulates convergent extension in the mouse embryo

María J. García-García1,2,*, Maho Shibata1 and Kathryn V. Anderson2

1 Molecular Biology and Genetics Department, Cornell University, Ithaca, NY 14853, USA.
2 Sloan Kettering Institute, New York, NY 10021, USA.

* Author for correspondence (e-mail: garciamj{at}cornell.edu)

Accepted 10 July 2008

In Xenopus and zebrafish embryos, elongation of the anterior-posterior body axis depends on convergent extension, a process that involves polarized cell movements and is regulated by non-canonical Wnt signaling. The mechanisms that control axis elongation of the mouse embryo are much less well understood. Here, we characterize the ENU-induced mouse mutation chato, which causes arrest at midgestation and defects characteristic of convergent extension mutants, including a shortened body axis, mediolaterally extended somites and an open neural tube. The chato mutation disrupts Zfp568, a Krüppel-associated box (KRAB) domain zinc-finger protein. Morphometric analysis revealed that the definitive endoderm of mouse wild-type embryos undergoes cell rearrangements that lead to convergent extension during early somite stages, and that these cell rearrangements fail in chato embryos. Although non-canonical Wnt signaling is important for convergent extension in the mouse notochord and neural plate, the results indicate that chato regulates body axis elongation in all embryonic tissues through a process independent of non-canonical Wnt signaling.

Key words: Axis elongation, Convergent extension, Definitive endoderm, Morphogenesis, Mouse development


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