Xiong W C, Montell C
Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Genes Dev. 1993 Jun;7(6):1085-96. doi: 10.1101/gad.7.6.1085.
Cell fate determination in the Drosophila eye is mediated by inductive events between neighboring cells in the eye imaginal disc. These inductive signals lead to differential gene expression necessary for the elaboration of different cell types in the compound eye. Several putative transcription factors have been identified previously that may be required for expression of genes that specify cell fate in the compound eye. Repression of inappropriate gene expression may be as important as transcriptional activation in the determination of cell fate. We report the identification of a mutation in the Drosophila tramtrack (ttk) locus that is required for cell fate determination in the compound eye. ttk is expressed as two proteins, p69 and p88, shown previously to bind to the regulatory regions of several segmentation genes. In ttk1, an allele missing the mRNA encoding p88, many ommatidia contained supernumerary R7 cells and decreased numbers of R1-R6 cells. ttk1e11, which appears to disrupt both Ttk proteins, was characterized by early embryonic arrest as well as transformation of ommatidial cells into nonommatidial cell types in mosaic flies. Consistent with previous proposals that the Ttk proteins are transcriptional repressors of segmentation genes, we detected ectopic or increased expression of the segment polarity gene engrailed in several ttk1 larval tissues. We propose that p69 is required to repress expression of genes that are incompatible with development of photoreceptor cell fates, whereas p88 appears to be required to repress genes that promote the R7 cell fate.
果蝇眼睛中的细胞命运决定是由眼成虫盘相邻细胞之间的诱导事件介导的。这些诱导信号导致差异基因表达,这对于复眼中不同细胞类型的形成是必需的。先前已经鉴定出几种假定的转录因子,它们可能是复眼中指定细胞命运的基因表达所必需的。在细胞命运决定中,抑制不适当的基因表达可能与转录激活同样重要。我们报告了在果蝇tramtrack(ttk)基因座中鉴定出一个突变,该突变是复眼中细胞命运决定所必需的。ttk表达为两种蛋白质,p69和p88,先前已证明它们与几个体节基因的调控区域结合。在ttk1中,一个缺失编码p88的mRNA的等位基因,许多小眼包含额外的R7细胞,而R1 - R6细胞数量减少。ttk1e11似乎破坏了两种Ttk蛋白,其特征是早期胚胎停滞以及在镶嵌果蝇中小眼细胞转变为非小眼细胞类型。与先前关于Ttk蛋白是体节基因转录抑制因子的提议一致,我们在几个ttk1幼虫组织中检测到了体节极性基因engrailed的异位或增加表达。我们提出p69是抑制与光感受器细胞命运发育不相容的基因表达所必需的,而p88似乎是抑制促进R7细胞命运的基因所必需的。