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© Fabrice Chrétien with Ultrapole, colorized by Jean-Marc Panaud
Cellule souche (en jaune) de muscle squelettique partiellement recouverte par la membrane basale, migrant sur une fibre musculaire (en bleu).
Publication : Development (Cambridge, England)

Bile system morphogenesis defects and liver dysfunction upon targeted deletion of HNF1beta

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Development (Cambridge, England) - 01 Apr 2002

Coffinier C, Gresh L, Fiette L, Tronche F, Schütz G, Babinet C, Pontoglio M, Yaniv M, Barra J

Link to Pubmed [PMID] – 11934849

Development 2002 Apr;129(8):1829-38

The inactivation of the Hnf1beta gene identified an essential role in epithelial differentiation of the visceral endoderm and resulted in early embryonic death. In the present study, we have specifically inactivated this gene in hepatocytes and bile duct cells using the Cre/loxP system. Mutant animals exhibited severe jaundice caused by abnormalities of the gallbladder and intrahepatic bile ducts (IHBD). The paucity of small IHBD was linked to a failure in the organization of duct structures during liver organogenesis, suggesting an essential function of Hnf1b in bile duct morphogenesis. Mutant mice also lacked interlobular arteries. As HNF1beta is not expressed in these cells, it further emphasizes the link between arterial and biliary formation. Hepatocyte metabolism was also affected and we identified hepatocyte-specific HNF1beta target genes involved in bile acids sensing and in fatty acid oxidation.

http://www.ncbi.nlm.nih.gov/pubmed/11934849