Liddell S, Bownes M
Department of Molecular Biology, University of Edinburgh, UK.
Mol Gen Genet. 1991 Aug;228(1-2):81-8. doi: 10.1007/BF00282451.
The three yolk proteins (YP1, YP2 and YP3) of Drosophila melanogaster are synthesized in two tissues of the adult female, the fat body and ovarian follicle cells. The YPs are selectively accumulated in the oocyte to provide nutrients for embryogenesis. We describe a female-sterile mutant, fs(1) A1526, which lacks YP3 in the haemolymph. The female sterility mutation mapped some distance away from the yp3 gene on the X chromosome and we were able to separate the YP3 defect from the female sterility by recombination, thus producing a fertile line of flies having no YP3 in the eggs. This shows that YP3 is not essential for embryogenesis. The mutant line is to be known as YP3s1. Investigation of yp3 transcription in the mutant females revealed that the gene is transcribed but yp3s1 mRNA levels are reduced relative to wild type. Transcription of the mutant yp3 gene can be induced in males by ecdysone. Investigation of the yolk proteins in YP3s1 females suggested that the YP3s1 polypeptide is synthesized in the fat body but not secreted. The mutant YP3 protein shows an increase in apparent molecular weight of approximately 1 kDa. The mutant yp3 gene was cloned and the DNA sequence determined. The sequence differences between the mutant and wild-type genes include an amino acid substitution in the leader sequence. We suggest that this may be responsible for the failure of YP3 secretion in the mutant YP3s1, and speculate on the cause of the reduction seen in the steady-state level of yp3 mRNA.
黑腹果蝇的三种卵黄蛋白（YP1、YP2和YP3）在成年雌性果蝇的两个组织中合成，即脂肪体和卵巢滤泡细胞。这些卵黄蛋白选择性地积累在卵母细胞中，为胚胎发育提供营养。我们描述了一种雌性不育突变体，fs(1) A1526，其血淋巴中缺乏YP3。该雌性不育突变位于X染色体上离yp3基因有一段距离的位置，我们能够通过重组将YP3缺陷与雌性不育分开，从而产生一种卵中没有YP3的可育果蝇品系。这表明YP3对胚胎发育不是必需的。该突变品系将被称为YP3s1。对突变雌性果蝇中yp3转录的研究表明，该基因能够转录，但相对于野生型，yp3s1的mRNA水平降低。突变的yp3基因的转录可在雄性果蝇中由蜕皮激素诱导。对YP3s1雌性果蝇的卵黄蛋白进行研究表明，YP3s1多肽在脂肪体中合成但未分泌。突变的YP3蛋白的表观分子量增加了约1 kDa。克隆了突变的yp3基因并测定了其DNA序列。突变基因与野生型基因之间的序列差异包括前导序列中的一个氨基酸替换。我们认为这可能是导致突变体YP3s1中YP3分泌失败的原因，并推测了yp3 mRNA稳态水平降低的原因。
