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doi: 10.1242/10.1242/dev.00176

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Development 130, 3-13 (2003)
Copyright © 2003 The Company of Biologists Limited

Node and midline defects are associated with left-right development in Delta1 mutant embryos

Gerhard K. H. Przemeck1,*, Ulrich Heinzmann2,*, Johannes Beckers1 and Martin Hrabé de Angelis1,{dagger}

1 GSF, Institute of Experimental Genetics, Ingolstaedter Landstr. 1, D-85764 Neuherberg, Germany
2 GSF, Institute of Pathology, Ingolstaedter Landstr. 1, D-85764 Neuherberg, Germany

{dagger} Author for correspondence (e-mail: hrabe{at}gsf.de)

Accepted 26 September 2002

Axes formation is a fundamental process of early embryonic development. In addition to the anteroposterior and dorsoventral axes, the determination of the left-right axis is crucial for the proper morphogenesis of internal organs and is evolutionarily conserved in vertebrates. Genes known to be required for the normal establishment and/or maintenance of left-right asymmetry in vertebrates include, for example, components of the TGF-ß family of intercellular signalling molecules and genes required for node and midline function. We report that Notch signalling, which previously had not been implicated in this morphogenetic process, is required for normal left-right determination in mice. We show, that the loss-of-function of the delta 1 (Dll1) gene causes a situs ambiguous phenotype, including randomisation of the direction of heart looping and embryonic turning. The most probable cause for this left-right defect in Dll1 mutant embryos is a failure in the development of proper midline structures. These originate from the node, which is disrupted and deformed in Dll1 mutant embryos. Based on expression analysis in wild-type and mutant embryos, we suggest a model, in which Notch signalling is required for the proper differentiation of node cells and node morphology.

Key words: Notch signalling, Gastrulation, Node formation, Notochord, Floorplate, Midline, Left-right asymmetry, Mouse


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