Genetic and biochemical evidence that gastrulation defects in Pofut2 mutants result from defects in ADAMTS9 secretion
详细信息 查看全文
- 作者：Brian A. Benza ; Sumeda Nandadasab ; Megumi Takeuchic ; Richard C. Gradya ; Hideyuki Takeuchic ; Rachel K. LoPilatoc ; Shinako Kakudaa ; Robert P.T. Somervilleb ; Suneel S. Apteb ; Robert S. Haltiwangerc ; rhalti@uga.edu" class="auth_mail" title="E-mail the corresponding author ; Bernadette C. Holdenera ; bernadette.holdener@stonybrook.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：O-Fucosylation ; Pofut2 ; Adamts9 ; Thrombospondin type I repeats ; Gastrulation
- 刊名：Developmental Biology
- 出版年：2016
- 出版时间：1 August 2016
- 年：2016
- 卷：416
- 期：1
- 页码：111-122
- 全文大小：14306 K
文摘
- •
Pofut2 and Adamts9 knockouts block gastrulation in mice.
- •
POFUT2 function in extraembryonic tissues is essential for gastrulation.
- •
Impaired secretion of ADAMTS9 likely blocks gastrulation in Pofut2 mutants.
- •
Loss of Pofut2 or Adamts9 in the epiblast impairs axis elongation.
- •
Defects in amnion and/or mesendoderm likely contribute to axis defects.