Gene Targeting Reveals a Widespread Role for the High-Mobility-Group Transcription Factor Sox11 in Tissue Remodeling
AUTOR(ES)
Sock, Elisabeth
FONTE
American Society for Microbiology
RESUMO
The high-mobility-group domain-containing transcription factor Sox11 is expressed transiently during embryonic development in many tissues that undergo inductive remodeling. Here we have analyzed the function of Sox11 by gene deletion in the mouse. Sox11-deficient mice died at birth from congenital cyanosis, likely resulting from heart defects. These included ventricular septation defects and outflow tract malformations that ranged from arterial common trunk to a condition known as double outlet right ventricle. Many other organs that normally express Sox11 also exhibited severe developmental defects. We observed various craniofacial and skeletal malformations, asplenia, and hypoplasia of the lung, stomach, and pancreas. Eyelids and the abdominal wall did not close properly in some Sox11-deficient mice. This phenotype suggests a prime function for Sox11 in tissue remodeling and identifies SOX11 as a potentially mutated gene in corresponding human malformation syndromes.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=444853Documentos Relacionados
- Idiopathic Weight Reduction in Mice Deficient in the High-Mobility-Group Transcription Factor Sox8
- The High-Mobility-Group Domain Transcription Factor Rop1 Is a Direct Regulator of prf1 in Ustilago maydis
- The role of intercalating residues in chromosomal high-mobility-group protein DNA binding, bending and specificity
- A testis-specific gene encoding a nuclear high-mobility-group box protein located in elongating spermatids.
- Mechanism of Regulatory Target Selection by the SOX High-Mobility-Group Domain Proteins as Revealed by Comparison of SOX1/2/3 and SOX9