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First published online 3 October 2007
doi: 10.1242/dev.004325

Development 134, 3789-3794 (2007)
Published by The Company of Biologists 2007
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Research Report

Mutations in the BMP pathway in mice support the existence of two molecular classes of holoprosencephaly

Marie Fernandes1, Grigoriy Gutin1, Heather Alcorn2, Susan K. McConnell3 and Jean M. Hébert1,*

1 Departments of Neuroscience and Molecular Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
2 Developmental Biology Program, Sloan-Kettering Institute, New York, NY 10021, USA.
3 Department of Biological Sciences, Stanford University, Stanford, CA, USA.

* Author for correspondence (e-mail: jhebert{at}aecom.yu.edu)

Accepted 29 August 2007

SUMMARY

Holoprosencephaly (HPE) is a devastating forebrain abnormality with a range of morphological defects characterized by loss of midline tissue. In the telencephalon, the embryonic precursor of the cerebral hemispheres, specialized cell types form a midline that separates the hemispheres. In the present study, deletion of the BMP receptor genes, Bmpr1b and Bmpr1a, in the mouse telencephalon results in a loss of all dorsal midline cell types without affecting the specification of cortical and ventral precursors. In the holoprosencephalic Shh-/- mutant, by contrast, ventral patterning is disrupted, whereas the dorsal midline initially forms. This suggests that two separate developmental mechanisms can underlie the ontogeny of HPE. The Bmpr1a;Bmpr1b mutant provides a model for a subclass of HPE in humans: midline inter-hemispheric HPE.

Key words: Telencephalon, Dorsal midline, Choroid plexus, Cortical hem, Holoprosencephaly, BMP, SHH




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