摘要
Homozygous
jumonji (
jmj
−/
jmj
−) mice were previously shown to exhibit hepatic hypoplasia and defective hematopoiesis in the liver and die at around embryonic day 15.5 (E15.5), suggesting that
jmj is essential for liver development. In order to gain insight into the mechanism of liver development, we analyzed the expression and function of
jmj in fetal hepatocytes. The number of hepatocytes in
jmj
−/
jmj
− mice was markedly reduced in comparison with control mice and the expression of
jmj in hepatocytes increased along with development. As
jmj
−/
jmj
− embryos die by E15.5, we employed an in vitro culture system in which fetal hepatocytes differentiate in response to oncostatin M. The proliferation potential of
jmj
−/
jmj
− hepatocytes was comparable to that of wild type cells in vitro, however maturation of hepatocytes as evidenced by the expression of liver enzymes such as tyrosine amino transferase was severely impaired by the
jmj gene inactivation. These results suggested that
jmj plays a pivotal role in the development of mid-fetal hepatocytes to the neonatal stage.