Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
15
pubmed:dateCreated
2006-7-12
pubmed:abstractText
Sonic hedgehog (SHH) is required to generate ventral cell types throughout the central nervous system. Its role in directly specifying ventral cells, however, has recently been questioned because loss of the Shh gene has little effect on ventral development if the Gli3 gene is also mutant. Consequently, another ventral determinant must exist. Here, genetic evidence establishes that FGFs are required for ventral telencephalon development. First, simultaneous deletion of Fgfr1 and Fgfr3 specifically in the telencephalon results in the loss of differentiated ventromedial cells; and second, in the Fgfr1;Fgfr2 double mutant, ventral precursor cells are lost, mimicking the phenotype obtained previously with a loss of SHH signalling. Yet, in the Fgfr1;Fgfr2 mutant, Shh remains expressed, as does Gli1, the transcription of which depends on SHH activity, suggesting that FGF signalling acts independently of SHH to generate ventral precursors. Moreover, the Fgfr1;Fgfr2 phenotype, unlike the Shh phenotype, is not rescued by loss of Gli3, further indicating that FGFs act downstream of Shh and Gli3 to generate ventral telencephalic cell types.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2937-46
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
FGF signalling generates ventral telencephalic cells independently of SHH.
pubmed:affiliation
Departments of Neuroscience and Molecular Genetics, Albert Einstein College of Medicine, 1410 Pelham Parkway South, Bronx, NY 10461, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural