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Pleiotropy of the Drosophila melanogaster foraging gene on larval feeding-related traits

机译:德罗洛拉美洛加斯族族觅食基因对幼虫喂养相关性状的胸膜炎

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Little is known about the molecular underpinning of behavioral pleiotropy. The Drosophila melanogaster foraging gene is highly pleiotropic, affecting many independent larval and adult phenotypes. Included in foraging's multiple phenotypes are larval foraging path length, triglyceride levels, and food intake. foraging has a complex structure with four promoters and 21 transcripts that encode nine protein isoforms of a cGMP dependent protein kinase (PKG). We examined if foraging's complex molecular structure underlies the behavioral pleiotropy associated with this gene. Using a promotor analysis strategy, we cloned DNA fragments upstream of each of foraging's transcription start sites and generated four separate for(pr)-Gal4s. Supporting our hypothesis of modular function, they had discrete, restricted expression patterns throughout the larva. In the CNS, for(pr1)-Gal4 and for(pr4)-Gal4 were expressed in neurons while for(pr2)-Gal4 and for(pr3)-Gal4 were expressed in glia cells. In the gastric system, for(pr1)-Gal4 and for(pr3)-Gal4 were expressed in enteroendocrine cells of the midgut while for(pr2)-Gal4 was expressed in the stem cells of the midgut. for(pr3)-Gal4 was expressed in the midgut enterocytes, and midgut and hindgut visceral muscle. for(pr4)-Gal4's gastric system expression was restricted to the hindgut. We also found promoter specific expression in the larval fat body, salivary glands, and body muscle. The modularity of foraging's molecular structure was also apparent in the phenotypic rescues. We rescued larval path length, triglyceride levels (bordered on significance), and food intake of for(0) null larvae using different for(pr)-Gal4s to drive UAS-for(cDNA). In a foraging null genetic background, for(pr1)-Gal4 was the only promoter driven Gal4 to rescue larval path length, for(pr3)-Gal4 altered triglyceride levels, and for(pr4)-Gal4 rescued food intake. Our results refine the spatial expression responsible for foraging's associated phenotypes, as well as the sub-regions of the locus responsible for their expression. foraging's pleiotropy arises at least in part from the individual contributions of its four promoters.
机译:关于行为肺炎的分子支撑性众所周知。果蝇觅食基因高度抗脂质,影响许多独立的幼虫和成人表型。包括在觅食的多种表型中是幼虫觅食路径长度,甘油三酯水平和食物摄入量。觅食具有复杂的结构,具有四种启动子和21种转录物,其编码CGMP依赖性蛋白激酶(PKG)的九种蛋白质同种型。我们检查了觅食的复杂分子结构是否下潜与该基因相关的行为胸膜。使用促进分析策略,我们克隆了每个觅食的转录开始网站上游的DNA片段,并为(PR)-GAL4S分开生成四个。支持我们的模块化功能的假设,它们在整个幼虫中具有离散的限制表达模式。在CNS中,对于(PR1)-GAL4和(PR4) - GAL4在神经元中表达,而对于(PR2)-GAL4和(PR3)-GAL4在胶质细胞中表达。在胃系系中,对于(Pr1) - GAL4和(PR3)-GAL4在中肠的肠道内分泌细胞中表达,同时在中肠的干细胞中表达(PR2)。对于(PR3) - GAL4在中肠肠细胞和中肠和后肠杆菌肌中表达。对于(PR4)-GAL4的胃系表达仅限于后肠。我们还发现幼虫体内,唾液腺和身体肌肉中的启动子特异性表达。在表型救援中,觅食的分子结构的模块性也显而易见。我们拯救了幼虫路径长度,甘油三酯水平(覆盖着显着性),以及使用不同的(0)Null幼虫的食物摄入(PR)-GAL4S驱动UAS(cDNA)。在觅食空遗传背景下,对于(PR1)-GAL4是唯一的启动子驱动的GAL4,用于拯救幼虫路径长度,用于(PR3) - GAL4改变的甘油三酯水平,并且对于(PR4)-GAL4救出的食物摄入量。我们的结果完善了负责觅食相关表型的空间表达,以及负责其表达的轨迹的子区域。觅食的胸膜复制至少部分地部分来自其四个启动子的个别贡献。

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