斑马鱼Dpr2通过促进节点受体的降解来抑制中胚层诱导。
Zebrafish Dpr2 inhibits mesoderm induction by promoting degradation of nodal receptors.
作者信息
Zhang Lixia, Zhou Hu, Su Ying, Sun Zhihui, Zhang Haiwen, Zhang Long, Zhang Yu, Ning Yuanheng, Chen Ye-Guang, Meng Anming
机构信息
Laboratory of Developmental Biology, Ministry of Education (MOE), Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, China.
出版信息
Science. 2004 Oct 1;306(5693):114-7. doi: 10.1126/science.1100569.
Nodal proteins, members of the transforming growth factor-beta (TGFbeta) superfamily, have been identified as key endogenous mesoderm inducers in vertebrates. Precise control of Nodal signaling is essential for normal development of embryos. Here, we report that zebrafish dapper2 (dpr2) is expressed in mesoderm precursors during early embryogenesis and is positively regulated by Nodal signals. In vivo functional studies in zebrafish suggest that Dpr2 suppresses mesoderm induction activities of Nodal signaling. Dpr2 is localized in late endosomes, binds to the TGFbeta receptors ALK5 and ALK4, and accelerates lysosomal degradation of these receptors.
Nodal蛋白是转化生长因子-β（TGFβ）超家族的成员，已被确定为脊椎动物中关键的内源性中胚层诱导因子。精确控制Nodal信号对于胚胎的正常发育至关重要。在此，我们报告斑马鱼dapper2（dpr2）在胚胎早期发育过程中在中胚层前体细胞中表达，并受到Nodal信号的正向调控。斑马鱼体内功能研究表明，Dpr2抑制Nodal信号的中胚层诱导活性。Dpr2定位于晚期内体，与TGFβ受体ALK5和ALK4结合，并加速这些受体的溶酶体降解。
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