Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-7-10
pubmed:abstractText
Sox9 encodes a HMG-box transcription factor that has been implicated in numerous developmental processes including chondrogenesis, formation of cardiac valves, and neural crest, testis and spinal cord development. Here we show that Sox9 is expressed in the notochord and the sclerotome during mouse development suggesting that the gene may play additional roles in the development of the axial skeleton. We used ubiquitous mosaic inactivation of a conditional Sox9 allele by Cre/loxP-mediated recombination in the mouse to screen for novel functions of Sox9, and revealed that its absence results in severe malformations of the vertebral column. Besides its established role in chondrogenesis, Sox9 is required for maintaining the structural integrity of the notochord. Mutant embryos establish a normal notochord; however, starting from E9.5, the notochord disintegrates in a cranial to caudal manner. The late requirement in notochord development uncovered a function of notochord-derived signals in inducing segmentation of the ventral sclerotome and chondrogenesis. Thus, Sox9 is required for axial skeletogenesis by regulating notochord survival and chondrogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0012-1606
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
295
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-40
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Sox9 is required for notochord maintenance in mice.
pubmed:affiliation
Institute of Human Genetics and Anthropology, University of Freiburg, D-79106 Freiburg, Germany. francisco.barrionuevo@uniklinik-freiburg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't