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First published online 29 March 2006
doi: 10.1242/dev.02346

Development 133, 1725-1734 (2006)
Published by The Company of Biologists 2006
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Lack of ß1 integrins in enteric neural crest cells leads to a Hirschsprung-like phenotype

Marie A. Breau1, Thomas Pietri1,*, Olivier Eder1, Martine Blanche1, Cord Brakebusch2, Reinhardt Fässler2, Jean P. Thiery1 and Sylvie Dufour1,{dagger}

1 UMR144, CNRS-Institut Curie, 26, rue d'Ulm, 75248 Paris cedex 05, France.
2 Max Planck Institute of Biochemistry, Department of Molecular Medicine, Martinsried, Germany.

{dagger} Author for correspondence (e-mail: sylvie.dufour{at}curie.fr)

Accepted 3 March 2006

The enteric nervous system arises mainly from vagal and sacral neural crest cells that colonise the gut between 9.5 and 14 days of development in mice. Using the Cre-LoxP system, we removed ß1 integrins in the neural crest cells when they emerge from the neural tube. ß1-null enteric neural crest cells fail to colonise the gut completely, leading to an aganglionosis of the descending colon, which resembles the human Hirschsprung's disease. Moreover, ß1-null enteric neural crest cells form abnormal aggregates in the gut wall, leading to a severe alteration of the ganglia network organisation. Organotypic cultures of gut explants reveal that ß1-null enteric neural crest cells show impaired adhesion on extracellular matrix and enhanced intercellular adhesion properties. They display migration defects in collagen gels and gut tissue environments. We also provide evidence that ß1 integrins are required for the villi innervation in the small intestine. Our findings highlight the crucial roles played by ß1 integrins at various steps of enteric nervous system development.

Key words: Enteric nervous system, ß1 integrins, Neural crest, Migration, Conditional knockout, Hirschsprung's disease, Mouse




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