Key Laboratory of Regenerative Biology, Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences, 510663 Guangzhou, China.
Dev Dyn. 2010 Aug;239(8):2198-207. doi: 10.1002/dvdy.22356.
An understanding of the molecular mechanisms governing the survival of organ progenitor cells in vivo is crucial for in vitro tissue regeneration. Here, we have found that Xenopus appl1 and akt2 share a similar embryonic expression pattern, showing characteristic expression in the central nervous system as well as in the pancreas and part of the stomach/duodenum (SD) at tadpole stages of development. Specific knockdown of appl1 in endoderm or inhibition of akt activity did not affect the formation of endodermal organ primordia at tail bud stages of development, but led to a gut-coiling defect, strong apoptosis in endodermal organs, and pancreas and SD hypoplasia or even aplasia at tadpole stages of development. Furthermore, appl1 is required for akt phosphorylation and akt2 in turn can rescue appl1 knockdown phenotypes. Together, our data suggest that appl1-akt signaling is specifically required for the survival of pancreas and SD progenitor cells in Xenopus laevis embryos.
了解控制器官祖细胞在体内存活的分子机制对于体外组织再生至关重要。在这里，我们发现 Xenopus appl1 和 akt2 具有相似的胚胎表达模式，在中枢神经系统以及在蝌蚪发育阶段的胰腺和部分胃/十二指肠（SD）中表现出特征性表达。在内胚层中特异性敲低 appl1 或抑制 akt 活性不会影响尾芽发育阶段内胚层器官原基的形成，但会导致肠卷曲缺陷、内胚层器官强烈凋亡以及在蝌蚪发育阶段胰腺和 SD 发育不良甚至缺失。此外，appl1 是 akt 磷酸化所必需的，而 akt2 反过来又可以挽救 appl1 敲低表型。总之，我们的数据表明，appl1-akt 信号通路对于 Xenopus laevis 胚胎中胰腺和 SD 祖细胞的存活是特异性必需的。
