In our previous study we demonstrated that the fruit ripening retardant Daminozide or Alar causes change in life history traits, distortion of adult wing structure, DNA damage in brain cells and mutagenic effects in fruit fly Drosophila melanogaster. As a continuation of the previous study the present work is designed to explore the metabolic modification of Daminozide following ingestion, the effects of Daminozide on the expression of genes which are pivotal for wing development and molecular interactions of Daminozide with those proteins involved in wing patterning. We demonstrated through reporter gene construct assay using X-gal staining method and transgenic Drosophila melanogaster stocks that the vestigial, wingless and decapentaplegic genes in wing imaginal disc from 3^rd instar larvae exhibited reduced expression when exposed to Daminozide in compare to control larvae. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) of those genes confirmed that exposure to Daminozide reduces the transcription level of those genes. In silico approach with molecular docking study revealed Daminozide may bind and interfere with the optimal functioning of expressed wing signaling proteins.

在我们之前的研究中，我们证明了水果成熟抑制剂Daminozide或Alar会导致生活史特征的改变，成年机翼结构的变形，脑细胞DNA的损伤以及果蝇果蝇的诱变作用。作为先前研究的延续，本研究旨在探索摄取后达米嗪的代谢修饰，达米嗪对机翼发育和与机翼构图有关的蛋白质的分子相互作用至关重要的基因表达的影响。通过使用X-gal染色法和转基因果蝇黑尾果种群的报告基因构建体测定，我们证明了残留的，无翅的和与对照幼虫相比，当暴露于Daminozide时，来自^第三龄幼虫幼虫翼状视盘中的decapentaplegic基因显示出降低的表达。这些基因的定量逆转录聚合酶链反应（qRT-PCR）证实，暴露于Daminozide会降低这些基因的转录水平。在分子对接研究的计算机方法中，达米诺嗪可能会结合并干扰表达的机翼信号蛋白的最佳功能。