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 for⁰ 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.

人们对行为多效性的分子基础知之甚少。果蝇觅食基因具有高度多效性，影响许多独立的幼虫和成虫表型。觅食的多种表型包括幼虫觅食路径长度、甘油三酯水平和食物摄入量。觅食具有复杂的结构，包含 4 个启动子和 21 个转录物，编码 cGMP 依赖性蛋白激酶 (PKG) 的 9 种蛋白亚型。我们检查了觅食的复杂分子结构是否是与该基因相关的行为多效性的基础。使用启动子分析策略，我们克隆了每个foraging转录起始位点上游的 DNA 片段，并为^pr -Gal4生成了四个单独的片段。支持我们的模块化功能假设，它们在整个幼虫中具有离散的、受限的表达模式。在CNS中，pr1 ^- Gal4和pr4 -Gal4^{在神经元中}表达，而pr2 -Gal4和pr3 -Gal4在神经胶质细胞中表达。在胃系统中，^{pr1-Gal4和pr3} - ^Gal4在中肠肠内分泌细胞中表达，而pr2 ^- Gal4在中肠干细胞中表达。pr3 -Gal4在中肠肠细胞、^中肠和后肠内脏肌中表达。^pr4 -Gal4的胃系统表达仅限于后肠。我们还在幼虫脂肪体、唾液腺和身体肌肉中发现了启动子特异性表达。觅食分子结构的模块化在表型救援中也很明显。^{我们使用不同的pr} -Gal4来驱动UAS-for ^cDNA ，挽救了0无效幼虫的幼虫路径长度、甘油三酯水平（接近显着性）和食物​​摄入^量。在觅食无效遗传背景中，pr1 ^-Gal4是驱动 Gal4 拯救幼虫路径长度的唯一启动子，^pr3 -Gal4改变甘油三酯水平，^pr4 -Gal4拯救食物摄入。我们的结果完善了负责觅食的空间表达的相关表型，以及负责其表达的基因座的子区域。觅食的多效性至少部分源于其四个启动子的个人贡献。