KIT is required for hepatic function during mouse post-natal development.
2007
Magnol, Laetitia | Chevallier, Marie-Clémence | Nalesso, Valérie | Retif, Stéphanie | Fuchs, Helmut | Klempt, Martina | Pereira, Patricia | Riottot, Michel | Andrzejewski, Sandra | Doan, Bich-Thuy | Panthier, Jean-Jacques | Puech, Anne | Beloeil, Jean-Claude | de Angelis, Martin Hrabe | Hérault, Yann | Institut de transgénose ; Centre National de la Recherche Scientifique (CNRS) | GSF research center ; Institute of Experimental Genetis | Neurobiologie de l'Olfaction et de la Prise Alimentaire (NOPA) ; Institut National de la Recherche Agronomique (INRA) | Consortium national de recherche en génomique (CNRG) ; Consortium national de recherche en génomique | Centre de biophysique moléculaire (CBM) ; Université d'Orléans (UO)-Université de Tours (UT)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut de Chimie - CNRS Chimie (INC-CNRS)-Centre National de la Recherche Scientifique (CNRS) | École nationale vétérinaire d'Alfort (ENVA) | CNRS, EUMORPHIA, EUROCOMP
International audience
اظهر المزيد [+] اقل [-]إنجليزي. BACKGROUND: The Kit gene encodes a receptor tyrosine kinase involved in various biological processes including melanogenesis, hematopoiesis and gametogenesis in mice and human. A large number of Kit mutants has been described so far showing the pleiotropic phenotypes associated with partial loss-of-function of the gene. Hypomorphic mutations can induce a light coat color phenotype while complete lack of KIT function interferes with embryogenesis. Interestingly several intermediate hypomorphic mutations induced in addition growth retardation and post-natal mortality. RESULTS: In this report we investigated the post-natal role of Kit by using a panel of chemically-induced hypomorphic mutations recently isolated in the mouse. We found that, in addition to the classical phenotypes, mutations of Kit induced juvenile steatosis, associated with the downregulation of the three genes, VldlR, Lpin1 and Lpl, controlling lipid metabolism in the post-natal liver. Hence, Kit loss-of-functions mimicked the inactivation of genes controlling the hepatic metabolism of triglycerides, the major source of energy from maternal milk, leading to growth and viability defects during neonatal development. CONCLUSION: This is a first report involving KIT in the control of lipid metabolism in neonates and opening new perspectives for understanding juvenile steatosis. Moreover, it reinforces the role of Kit during development of the liver and underscores the caution that should be exerted in using KIT inhibitors during anti-cancer treatment.
اظهر المزيد [+] اقل [-]الكلمات المفتاحية الخاصة بالمكنز الزراعي (أجروفوك)
المعلومات البيبليوغرافية
تم تزويد هذا السجل من قبل Institut national de la recherche agronomique