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<p>The fruit fly, <i>Drosophila melanogaster</i>, is a valuable model for studying the mechanisms of chemosensation. The odorant receptor Or56a has been shown to be narrowly tuned to geosmin—a chemical that flies use as a proxy for toxic molds and bacteria—and its activation drives olfactory avoidance behavior. Here, I find that existing <i>Gal4</i> drivers using cloned promoter fragments of the <i>Or56a</i> gene drive unexpected expression in the labral sense organ (LSO), an internal taste sensory organ within the fly pharynx, in addition to their reported expression in the olfactory antennae. However, the presence of geosmin in sucrose solution does not elicit taste aversion or reduce consumption. Furthermore, a knock-in <i>Or56a-T2A-Gal4</i> line newly generated in this study does not drive expression in the LSO. These results suggest that the LSO expression likely reflects ectopic expression from the existing <i>Or56a-Gal4</i> drivers rather than the endogenous <i>Or56a</i> expression pattern. This study adds to the growing evidence that genetic drivers constructed using cloned promoters may not always faithfully recapitulate endogenous gene expression patterns, which should be taken into consideration when interpreting experimental results.</p>

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Gal4 drivers of the geosmin receptor Or56a exhibit ectopic expression in the labral sense organ of Drosophila

  • 期刊论文

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  • 发表日期：

    2025年8月27日

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  • Zepeng Yao

摘要

The fruit fly, Drosophila melanogaster, is a valuable model for studying the mechanisms of chemosensation. The odorant receptor Or56a has been shown to be narrowly tuned to geosmin—a chemical that flies use as a proxy for toxic molds and bacteria—and its activation drives olfactory avoidance behavior. Here, I find that existing Gal4 drivers using cloned promoter fragments of the Or56a gene drive unexpected expression in the labral sense organ (LSO), an internal taste sensory organ within the fly pharynx, in addition to their reported expression in the olfactory antennae. However, the presence of geosmin in sucrose solution does not elicit taste aversion or reduce consumption. Furthermore, a knock-in Or56a-T2A-Gal4 line newly generated in this study does not drive expression in the LSO. These results suggest that the LSO expression likely reflects ectopic expression from the existing Or56a-Gal4 drivers rather than the endogenous Or56a expression pattern. This study adds to the growing evidence that genetic drivers constructed using cloned promoters may not always faithfully recapitulate endogenous gene expression patterns, which should be taken into consideration when interpreting experimental results.