Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-9-15
pubmed:abstractText
The formation of supernumerary digits, or polydactyly, is a common congenital malformation. Although mutations in a number of genes have been linked to polydactyly, the molecular etiology for a third of human disorders with polydactyly remains unknown. To increase our understanding of the potential causes for polydactyly, we characterized a spontaneous chicken mutant, known as Dorking. The hindlimbs of Dorkings form a preaxial supernumerary digit. During the early stages of limb development, ectopic expression of several genes, including Sonic Hedgehog (Shh) and Fibroblast Growth Factor 4 (Fgf4), was found in Dorking hindlimbs. In addition to ectopic gene expression, a decrease in cell death in the anterior of the developing Dorking hindlimb was observed. Further molecular investigation revealed that ectopic Fgf4 expression was initiated and maintained independent of ectopic Shh. Additionally, inhibition of Fgf signaling but not hedgehog signaling was capable of restoring the normal anterior domain of cell death in Dorking hindlimbs. Our data indicates that in Dorking chickens, preaxial polydactyly is initiated independent of Shh.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1095-564X
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
334
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
133-41
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Aberrant FGF signaling, independent of ectopic hedgehog signaling, initiates preaxial polydactyly in Dorking chickens.
pubmed:affiliation
Department of Molecular Genetics and Microbiology, The Genetics Institute, University of Florida, Gainesville, FL 32610, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't