Hart K, Klein T, Wilcox M
MRC Laboratory of Molecular Biology, Cambridge, UK.
Mech Dev. 1993 Oct;43(2-3):101-10. doi: 10.1016/0925-4773(93)90028-v.
E(Dl)KP135 has been isolated previously as a recessive lethal Drosophila P element insertion line with a dominant enhancing effect on the phenotype of Delta, a gene encoding a surface membrane protein. We show here that this P insertion also enhances the wing phenotype of nd1, an allele of Notch encoding another transmembrane protein, the putative receptor of Delta, as well as that of if3, an allele of the integrin gene PS2 alpha. Moreover, we noticed that this P insertion causes a severe Minute phenotype. Molecular characterisation revealed that the P element disrupts the putative mRNA leader sequence of the ribosomal protein L19 gene. We tested further Minute genes and found that two of them, similarly to E(Dl)KP135, strongly enhance the nd1 wing phenotype. Our results suggest that the pleiotropic Minute syndrome can affect, probably indirectly, one or more steps of wing morphogenesis that involve surface adhesion of epithelial cells.
E(Dl)KP135先前已作为一种隐性致死的果蝇P因子插入系被分离出来，它对Delta（一种编码表面膜蛋白的基因）的表型具有显性增强作用。我们在此表明，这种P因子插入还增强了Notch的一个等位基因nd1（编码另一种跨膜蛋白，即Delta的假定受体）以及整合素基因PS2α的一个等位基因if3的翅表型。此外，我们注意到这种P因子插入会导致严重的小翅脉表型。分子特征分析表明，P因子破坏了核糖体蛋白L19基因的假定mRNA前导序列。我们进一步测试了其他小翅脉基因，发现其中两个基因与E(Dl)KP135类似，强烈增强了nd1的翅表型。我们的结果表明，多效性小翅脉综合征可能间接影响翅形态发生的一个或多个步骤，这些步骤涉及上皮细胞的表面黏附。
