Linked Life Data

15217086

Source:http://linkedlifedata.com/resource/pubmed/id/15217086

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-6-25
pubmed:abstractText
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-3069
pubmed:author
pubmed:issnType
Print
pubmed:volume
63
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
574-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Msx1-deficient mice fail to form prosomere 1 derivatives, subcommissural organ, and posterior commissure and develop hydrocephalus.
pubmed:affiliation
Departamento de Biología Celular, Genética y Fisiología, Facultad de Ciencias, Universidad de Málaga, Málaga, Spain. llebrez@uma.es
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't