Giniger E, Tietje K, Jan L Y, Jan Y N
Fred Hutchinson Cancer Research Center, Seattle, WA 98104.
Development. 1994 Jun;120(6):1385-98. doi: 10.1242/dev.120.6.1385.
Mutations in the gene longitudinals lacking (lola) lead to defects in the development of axon tracts in the Drosophila embryonic central nervous system. We now show that lola mutations also cause defects of axon growth and guidance in the peripheral nervous system, and causes a particular cluster of embryonic sense organs (lch5) to be oriented improperly. Axonal aberrations caused by lola are similar to those caused by mutations of three other genes, logo, Notch and Delta, raising the possibility that lola works in the same genetic pathway as do these other molecules. The lola gene encodes at least two nuclear protein products, apparently by differential RNA splicing. The predicted proteins contain an amino-terminal motif similar to that recently described for a family of transcription factors, including the products of the Drosophila genes tramtrack and the Broad Complex. Like Ttk and BR-C, one of the two characterized products of the lola locus bears sequences similar to the zinc-finger motif, but the other (neuronal) form of the protein has no recognizable DNA-binding motif.
“缺少纵向(lola)”基因的突变会导致果蝇胚胎中枢神经系统中轴突束发育缺陷。我们现在表明,lola突变还会导致外周神经系统中轴突生长和导向缺陷,并使一群特定的胚胎感觉器官(lch5)定向异常。lola引起的轴突畸变与其他三个基因logo、Notch和Delta的突变所导致的畸变相似,这增加了lola与这些其他分子在相同遗传途径中起作用的可能性。lola基因显然通过差异RNA剪接编码至少两种核蛋白产物。预测的蛋白质含有一个氨基末端基序,类似于最近描述的一类转录因子,包括果蝇基因tramtrack和Broad Complex的产物。与Ttk和BR-C一样,lola位点的两个已鉴定产物之一带有与锌指基序相似的序列,但该蛋白质的另一种(神经元)形式没有可识别的DNA结合基序。