Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Fernández-Llebrez, P. et al.

Fernández-Llebrez, Grondona, Pérez, López-Aranda, Estivill-Torrús, Llebrez-Zayas, Soriano, Ramos, Lallemand, Bach, Robert,

Msx1-deficient mice fail to form prosomere 1 derivatives, subcommissural organ, and posterior commissure and develop hydrocephalus.

Msx1 is a regulatory gene involved in epithelio-mesenchymal interactions in limb formation and organogenesis. In the embryonic CNS, the Msx1 gene is expressed along the dorsal midline. Msx1 mutant mice have been obtained by insertion of the nlacZ gene in the Msx1 homeodomain. The most important features of homozygous mutants that we observed were the absence or malformation of the posterior commissure (PC) and of the subcommissural organ (SCO), the collapse of the cerebral aqueduct, and the development of hydrocephalus. Heterozygous mutants developed abnormal PC and reduced SCO, as revealed by specific antibodies against SCO secretory glycoproteins. About one third of the heterozygous mutants also showed hydrocephalus. Other defects displayed by homozygous mutants were ependymal denudation, subventricular cavitations and edema, and underdevelopment of the pineal gland and subfornical organ. Some homozygous mutants developed both SCO and PC, probably as a consequence of genetic redundancy with Msx2. However, these mutants did not show SCO-immunoreactive glycoproteins and displayed obstructive hydrocephalus. This suggests that Msx1 is necessary for the synthesis of SCO glycoproteins, which would then be required for the maintenance of an open aqueduct.[1]

References

Msx1-deficient mice fail to form prosomere 1 derivatives, subcommissural organ, and posterior commissure and develop hydrocephalus. Fernández-Llebrez, P., Grondona, J.M., Pérez, J., López-Aranda, M.F., Estivill-Torrús, G., Llebrez-Zayas, P.F., Soriano, E., Ramos, C., Lallemand, Y., Bach, A., Robert, B. J. Neuropathol. Exp. Neurol. (2004) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.