Cell fate specification in gastrointestinal epithelial cells by helix-loop-helix factor Id2

螺旋-环-螺旋因子Id2对胃肠道上皮细胞的细胞命运规范

• 批准号: 24790194
• 负责人: MORI Kentaro
• 金额: $ 2.91万
• 依托单位: University of Fukui
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2012
• 资助国家: 日本
• 起止时间: 2012-04-01 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-24790194/
• 关键词: 細胞分化; 消化管上皮; 内胚葉; 転写因子; Id2; Irx3; Irx5; 消化管; 上皮細胞; 国際情報交換; 細胞分化; 消化管上皮; 内胚葉; 転写因子; Id2; Irx3; Irx5; 消化管; 上皮細胞; 国際情報交換

Gastrointestinal epithelial cells are derived from endoderm, and region-specific endoderm differentiation establishes the functionally distinct organ, esophagus, stomach and caudally positioned intestine. How region-specific epithelial characteristics are generated during development remains poorly understood. I have found that the knockout mice of transcriptional repressor Id2 develop intestinal tumors, and revealed that the tumors are derived from ectopic gastric tissues formed in the small intestine during development. This study demonstrates that Id2 is involved in the cell fate specification of the intestinal epithelial cells through the suppression of the foregut endoderm genes expression.

胃肠道上皮细胞源自内胚层，特异性内胚层分化建立了功能上不同的器官，食管，胃和尾肠。在发育过程中如何产生区域特异性上皮特征仍然知之甚少。我发现转录阻遏物ID2的敲除小鼠会发生肠道肿瘤，并揭示了肿瘤是从发育过程中小肠中形成的异位胃组织衍生的。这项研究表明，ID2通过抑制前肠内胚层基因的表达参与了肠上皮细胞的细胞命运规范。