Fortini M E, Simon M A, Rubin G M
Howard Hughes Medical Institute, University of California, Berkeley 94720.
Nature. 1992 Feb 6;355(6360):559-61. doi: 10.1038/355559a0.
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. The sev gene encodes a receptor protein tyrosine kinase (Sev) localized on the R7 surface, activated by a boss-encoded ligand presented by R8. The sina gene encodes a nuclear factor required in R7. 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. We report here that Ras1 activation may account for all of the signalling action of Sev; an activated Ras1Va112 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.
在发育中的果蝇眼睛里，R7光感受器的细胞命运特化依赖于来自相邻R8细胞的诱导信号。三个基因——无七（sev）、无七之妻（boss）和失七（sina）——发生突变会导致R7前体细胞变成非神经的视锥细胞。sev基因编码一种定位在R7表面的受体蛋白酪氨酸激酶（Sev），它被R8细胞呈递的由boss基因编码的配体激活。sina基因编码R7中所需的一种核因子。Ras1基因剂量的减少会损害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。我们在此报告，Ras1的激活可能解释了Sev的所有信号传导作用；一个激活的Ras1Va112蛋白能挽救sev和boss基因缺失突变体中正常的R7前体，使其不转变为视锥细胞，并诱导形成额外的R7细胞。果蝇Ras2蛋白的类似激活不会产生这些效应，这证明了Ras蛋白的特异性。
