Notochord repression of endodermal Sonic hedgehog permits pancreas development
Notochord repression of endodermal Sonic hedgehog permits pancreas development
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DOI：
10.1101/gad.12.11.1705
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发表时间：
1998-06-01
影响因子：
10.5
通讯作者：
Melton, DA
中科院分区：
文献类型：
--
作者：
Hebrok, M;Kim, SK;Melton, DA
鸡背胰的发育需要脊索向内胚层发出信号。音速刺猬（SHH）通常是不存在的胰腺内胚层，我们提供的证据表明，脊索，相反，其对邻近神经外胚层的SHH表达诱导，抑制SKH表达在邻近新生胰腺内胚层。我们确定激活素β B和FGF 2作为脊索因子，可以抑制内胚层SHH，从而允许胰腺基因（包括Pdx 1和胰岛素）的表达。用阻断hedgehog活性的抗体治疗内胚层也导致胰腺基因表达。通过细胞间信号，如激活素和FGF，防止SHH在前胰腺背内胚层的表达，可能是允许鸡胰腺发育早期步骤的关键。
Notochord signals to the endoderm are required for development of the chick dorsal pancreas. Sonic hedgehog (SHH) is normally absent from pancreatic endoderm, and we provide evidence that notochord, in contrast to its effects on adjacent neuroectoderm where SHH expression is induced, represses SKH expression in adjacent nascent pancreatic endoderm. We identify activin-beta B and FGF2 as notochord factors that can repress endodermal SHH and thereby permit expression of pancreas genes including Pdx1 and insulin. Endoderm treatment with antibodies that block hedgehog activity also results in pancreatic gene expression. Prevention of SHH expression in prepancreatic dorsal endoderm by intercellular signals, like activin and FGF, may be critical for permitting early steps of chick pancreatic development.