Coactivation of STAT and Ras is required for germ cell proliferation and invasive migration in Drosophila
Coactivation of STAT and Ras is required for germ cell proliferation and invasive migration in Drosophila
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DOI：
10.1016/s1534-5807(03)00328-9
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发表时间：
2003-11-01
影响因子：
11.8
通讯作者：
Li, X
中科院分区：
文献类型：
--
作者：
Li, JH;Xia, F;Li, X
原始生殖细胞（PGC）经历增殖、侵袭、引导迁移和聚集形成性腺。在这里，我们发现，在果蝇中，受体酪氨酸激酶 Torso 在 PGC 发育的早期阶段同时激活 STAT 和 Ras，并且 STAT 和 Ras 的共同激活是 PGC 增殖和侵袭性迁移所必需的。 stat92E 或 Ras1 的胚胎突变体具有较少的 PGC，并且这些细胞迁移缓慢、错误，并且无法合并。相反，这些分子的过度激活会导致多余的 PGC、它们过早地穿过肠道上皮以及异位定植。果蝇 PGC 发育对 RTK 的要求类似于小鼠，其中需要 RTK c-kit，这表明在果蝇和哺乳动物中控制 PGC 行为的保守分子机制。
Primordial germ cells (PGCs) undergo proliferation, invasion, guided migration, and aggregation to form the gonad. Here we show that in Drosophila, the receptor tyrosine kinase Torso activates both STAT and Ras during the early phase of PGC development, and co-activation of STAT and Ras is required for PGC proliferation and invasive migration. Embryos mutant for stat92E or Ras1 have fewer PGCs, and these cells migrate slowly, errantly, and fail to coalesce. Conversely, overactivation of these molecules causes supernumerary PGCs, their premature transit through the gut epithelium, and ectopic colonization. A requirement for RTK in Drosophila PGC development is analogous to the mouse, in which the RTK c-kit is required, suggesting a conserved molecular mechanism governing PGC behavior in flies and mammals.