SIGNALING BY THE SEVENLESS PROTEIN TYROSINE KINASE IS MIMICKED BY RAS1 ACTIVATION
SIGNALING BY THE SEVENLESS PROTEIN TYROSINE KINASE IS MIMICKED BY RAS1 ACTIVATION
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DOI：
10.1038/355559a0
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发表时间：
1992-02-06
期刊：
影响因子：
64.8
通讯作者：
RUBIN, GM
中科院分区：
文献类型：
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作者：
FORTINI, ME;SIMON, MA;RUBIN, GM
发育中的果蝇眼睛中R7光感受器的CELL-FATE规范依赖于邻近R8细胞的感应信号。七个少的（sev），七个少的新娘（boss）和七个缺席的（sina）三个基因的突变导致R7前体成为非神经锥体细胞1-3。sev基因编码位于R7表面的受体蛋白酪氨酸激酶（sev），由R8呈递的boss编码配体激活（参考文献4-6）。sina基因编码R7所需的核因子（参考文献3）。减少Ras1基因的剂量会损害Sev介导的信号传导，这表明Ras1的激活可能是Sev激活的一个重要结果7。我们在这里报道，Ras1激活可能解释了Sev的所有信号传导作用；激活的Ras1Val12蛋白使正常的R7前体在sev和boss零突变体中转化为锥细胞，并诱导形成多余的R7细胞。果蝇Ras2蛋白的类似激活不会产生这些作用，这表明Ras蛋白具有特异性。
CELL-FATE specification of R7 photoreceptors in the developing Drosophila eye depends on an inductive signal from neighbouring R8 cells. Mutations in three genes, sevenless (sev), bride-of-sevenless (boss) and seven-in-absentia (sina) cause the R7 precursor to become a non-neural cone cell 1-3. The sev gene encodes a receptor protein tyrosine kinase (Sev) localized on the R7 surface, activated by a boss-encoded ligand presented by R8 (refs 4-6). The sina gene encodes a nuclear factor required in R7 (ref. 3). Reduction in the dosage of the Ras1 gene impairs Sev-mediated signalling, suggesting that activation of Ras1 may be an important consequence of Sev activation 7. We report here that Ras1 activation may account for all of the signalling action of Sev; an activated Ras1Val12 protein rescues the normal R7 precursor from transformation into a cone cell in sev and boss null mutants and induces the formation of supernumerary R7 cells. Similar activation of the Drosophila Ras2 protein does not produce these effects, demonstrating Ras protein specificity.