TY - JOUR
T1 - Expression and function of mouse Sox17 gene in the specification of gallbladder/bile-duct progenitors during early foregut morphogenesis
AU - Uemura, Mami
AU - Hara, Kenshiro
AU - Shitara, Hiroshi
AU - Ishii, Rie
AU - Tsunekawa, Naoki
AU - Miura, Yutaroh
AU - Kurohmaru, Masamichi
AU - Taya, Choji
AU - Yonekawa, Hiromichi
AU - Kanai-Azuma, Masami
AU - Kanai, Yoshiakira
N1 - Funding Information:
The authors wish to thank Prof. Drs. Patrick P. Tam (Univ. of Sydney, Australia), Nobuyoshi Shiojiri (Shizuoka Univ., Japan) and Yukio Saijoh (Univ. of Utah, USA) for their kind critical reading on the manuscript. This work was supported by financial grants from the Ministry of Education, Science, Sports and Culture of Japan to Y. Kanai (B-19380168 and A-21248034) and M. Kanai-Azuma (C-70321883).
PY - 2010/1/1
Y1 - 2010/1/1
N2 - In early-organogenesis-stage mouse embryos, the posteroventral foregut endoderm adjacent to the heart tube gives rise to liver, ventral pancreas and gallbladder. Hepatic and pancreatic primordia become specified in the posterior segment of the ventral foregut endoderm at early somite stages. The mechanisms for demarcating gallbladder and bile duct primordium, however, are poorly understood. Here, we demonstrate that the gallbladder and bile duct progenitors are specified in the paired lateral endoderm domains outside the heart field at almost the same timing as hepatic and pancreatic induction. In the anterior definitive endoderm, Sox17 reactivation occurs in a certain population within the most lateral domains posterolateral to the anterior intestinal portal (AIP) lip on both the left and right sides. During foregut formation, the paired Sox17-positive domains expand ventromedially to merge in the midline of the AIP lip and become localized between the liver and pancreatic primordia. In Sox17-null embryos, these lateral domains are missing, resulting in a complete loss of the gallbladder/bile-duct structure. Chimera analyses revealed that Sox17-null endoderm cells in the posteroventral foregut do not display any gallbladder/bile-duct molecular characters. Our findings show that Sox17 functions cell-autonomously to specify gallbladder/bile-duct in the mouse embryo.
AB - In early-organogenesis-stage mouse embryos, the posteroventral foregut endoderm adjacent to the heart tube gives rise to liver, ventral pancreas and gallbladder. Hepatic and pancreatic primordia become specified in the posterior segment of the ventral foregut endoderm at early somite stages. The mechanisms for demarcating gallbladder and bile duct primordium, however, are poorly understood. Here, we demonstrate that the gallbladder and bile duct progenitors are specified in the paired lateral endoderm domains outside the heart field at almost the same timing as hepatic and pancreatic induction. In the anterior definitive endoderm, Sox17 reactivation occurs in a certain population within the most lateral domains posterolateral to the anterior intestinal portal (AIP) lip on both the left and right sides. During foregut formation, the paired Sox17-positive domains expand ventromedially to merge in the midline of the AIP lip and become localized between the liver and pancreatic primordia. In Sox17-null embryos, these lateral domains are missing, resulting in a complete loss of the gallbladder/bile-duct structure. Chimera analyses revealed that Sox17-null endoderm cells in the posteroventral foregut do not display any gallbladder/bile-duct molecular characters. Our findings show that Sox17 functions cell-autonomously to specify gallbladder/bile-duct in the mouse embryo.
KW - Bile duct
KW - Endoderm
KW - Gallbladder
KW - Mouse
KW - Pancreas
KW - Sox17
UR - http://www.scopus.com/inward/record.url?scp=72949097848&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=72949097848&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2009.11.063
DO - 10.1016/j.bbrc.2009.11.063
M3 - Article
C2 - 19913509
AN - SCOPUS:72949097848
VL - 391
SP - 357
EP - 363
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 1
ER -