Bender M, Turner F R, Kaufman T C
Dev Biol. 1987 Feb;119(2):418-32. doi: 10.1016/0012-1606(87)90046-7.
We report the characterization of loss-of-function alleles of the homoeotic mutation Regulator of postbithorax (Rg-pbx) in Drosophila melanogaster. Rg-pbx is a dominant gain-of-function mutation which shows a transformation of posterior haltere to wing in the adult cuticle. This mutant phenotype mimics that of the bithorax complex lesion postbithorax (pbx). Loss-of-function alleles described here are lethal in the embryonic stage and affect the pattern of segmentation of the embryo. Examination of the terminal phenotype of null and hypomorphic alleles of Rg-pbx has shown that inactivation of the Rg-pbx gene leads to loss of the thoracic segments and the adjacent labial segment of the Drosophila embryo. An effect of the mutations is also seen in the seventh and eighth abdominal segments of embryos. The loss-of-function phenotype is similar to that described for the segmentation mutant hunchback (hb). Complementation tests show that Rg-pbx and hb are allelic. Temperature shift experiments using a temperature-sensitive loss-of-function allele show that the Rg-pbx gene product is required early in embryogenesis. We further report that the dominant Rg-pbx phenotype is sensitive to the gene dosage of another segmentation-controlling gene, fushi tarazu (ftz). Flies carrying a mutant copy of the ftz gene in trans to Rg-pbx show a dramatic enhancement of the penetrance of the homoeotic mutant phenotype. We were also able to demonstrate a suppression of the Rg-pbx phenotype by the addition of a duplication for the ftz+ gene to an Rg-pbx stock. Examination of the phenotype of ftz Rg-pbx- double-mutant embryos did not reveal a clear pattern of epistasis between the genes nor was absolute additivity of phenotype seen. A possible formal relationship between Rg-pbx, ftz, and the postbithorax (pbx) locus is proposed.
我们报道了黑腹果蝇中同源异型突变后胸调节因子（Rg-pbx）功能缺失等位基因的特征。Rg-pbx是一个显性功能获得性突变，在成虫表皮中表现为后翅转化为翅。这种突变表型与双胸复合体病变后胸（pbx）的表型相似。本文描述的功能缺失等位基因在胚胎期是致死的，并影响胚胎的体节模式。对Rg-pbx无效和亚效等位基因的终末表型检查表明，Rg-pbx基因的失活导致果蝇胚胎胸节和相邻唇节的缺失。在胚胎的第七和第八腹节也观察到了突变的影响。功能缺失表型与节段突变驼背（hb）所描述的表型相似。互补试验表明Rg-pbx和hb是等位基因。使用温度敏感型功能缺失等位基因进行的温度转换实验表明，Rg-pbx基因产物在胚胎发育早期是必需的。我们进一步报道，显性Rg-pbx表型对另一个节段控制基因腹足不足（ftz）的基因剂量敏感。携带与Rg-pbx反式的ftz基因突变拷贝的果蝇显示，同源异型突变表型的外显率显著提高。我们还能够通过向Rg-pbx品系添加ftz+基因的重复片段来证明对Rg-pbx表型的抑制。对ftz Rg-pbx双突变胚胎的表型检查没有揭示基因之间明确的上位性模式，也没有观察到表型的绝对加性。提出了Rg-pbx、ftz和后胸（pbx）位点之间可能的形式关系。
