Linked Life Data

12217321

Source:http://linkedlifedata.com/resource/pubmed/id/12217321

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-9-9
pubmed:abstractText
The Hox genes encode a group of transcription factors essential for proper development of the mouse. Targeted mutation of the Hoxd11 gene causes reduced male fertility, vertebral transformation, carpal bone fusions, and reductions in digit length. A duplication of the Hoxd11 gene was created with the expectation that the consequences of restricted overexpression in the appropriate cells would provide further insight into the function of the Hoxd11 gene product. Genetic assays demonstrated that two tandem copies of Hoxd11 were functionally indistinguishable from the normal two copies of the gene on separate chromosomes with respect to formation of the axial and appendicular skeleton. Extra copies of Hoxd11 caused an increase in the lengths of some bones of the forelimb autopod and a decrease in the number of lumbar vertebrae. Further, analysis of the Hoxd11 duplication demonstrated that the Hoxd11 protein can perform some functions supplied by its paralogue Hoxa11. For example, the defects in forelimb bones are corrected when extra copies of Hoxd11 are present in the Hoxa11 homozygous mutant background. Thus, it appears that Hoxd11 can quantitatively compensate for the absence of Hoxa11 protein, and therefore Hoxa11 and Hoxd11 are functionally equivalent in the zeugopod. However, extra copies of Hoxd11 did not improve male or female fertility in Hoxa11 mutants. Interestingly, the insertion of an additional Hoxd11 locus into the HoxD complex does not appear to affect the expression patterns of the neighboring Hoxd10, -d12, or -d13 genes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0012-1606
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
249
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
96-107
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12217321-Animals, pubmed-meshheading:12217321-Bone Development, pubmed-meshheading:12217321-Bone and Bones, pubmed-meshheading:12217321-Embryo, Mammalian, pubmed-meshheading:12217321-Female, pubmed-meshheading:12217321-Forelimb, pubmed-meshheading:12217321-Gene Duplication, pubmed-meshheading:12217321-Gene Expression Regulation, Developmental, pubmed-meshheading:12217321-Gene Order, pubmed-meshheading:12217321-Genetic Complementation Test, pubmed-meshheading:12217321-Homeodomain Proteins, pubmed-meshheading:12217321-Homozygote, pubmed-meshheading:12217321-Male, pubmed-meshheading:12217321-Mice, pubmed-meshheading:12217321-Mice, Mutant Strains, pubmed-meshheading:12217321-Oncogene Proteins, pubmed-meshheading:12217321-Reproduction, pubmed-meshheading:12217321-Skeleton, pubmed-meshheading:12217321-Transcription Factors, pubmed-meshheading:12217321-Zebrafish Proteins
pubmed:year
2002
pubmed:articleTitle
Duplication of the Hoxd11 gene causes alterations in the axial and appendicular skeleton of the mouse.
pubmed:affiliation
Howard Hughes Medical Institute, Department of Human Genetics, University of Utah, School of Medicine, Salt Lake City, Utah 84112-5331, USA.
pubmed:publicationType
Journal Article