UC Riverside

Eukaryotes are frequently exposed to microbes and their secreted metabolites, including volatile odor compounds (VOCs). However, the effects of long-term exposure to these microbial volatiles, and other environmental volatiles remain largely unexplored. This study uses Drosophila melanogaster, Arabidopsis thaliana, and human cell lines as model systems to investigate the impact of VOCs such as diacetyl, a volatile emitted by yeast found around fermenting fruits. The findings reveal that exposure to diacetyl vapors alone can alter gene expression in the antenna of Drosophila. Diacetyl and related compounds also inhibit human histone-deacetylases (HDACs), increase histone-H3K9 acetylation in human cells, and induce widespread changes in gene expression in both Drosophila and mice. Notably, diacetyl crosses the blood-brain barrier and modulates gene expression in the brain, indicating its potential as a therapeutic agent.The study further explores the physiological effects of volatile exposure using two disease models responsive to HDAC inhibitors. Diacetyl vapors were found to inhibit the proliferation of human neuroblastoma cells in culture and slow neurodegeneration in a Drosophila model of Huntington’s disease. These findings suggest that certain environmental volatiles can profoundly impact histone acetylation, gene expression, and physiology in animals, potentially without our awareness. In addition to animals, volatile odor compounds play a significant role in plant communities, influencing development and stress responses. The study demonstrates that specific VOCs can cause notable changes in plant root growth, leaf development, and flowering time by altering gene expression through HDAC inhibition pathways. These epigenetic changes also affect how plants respond to abiotic stressors such as freezing. The research highlights a potentially conserved pathway in eukaryotes, including plants, for responding to environmental volatiles. Furthermore, we study interaction of odorants with transmembrane odorant receptor proteins. Using Aedes aegypti co-receptor mutants for two different chemoreceptor gene families, Gustatory Receptors (Gr3), Ionotropic Receptors (Ir76b and Ir25a). Specifically, I assessed how the maxillary palp CO2 receptor neurons rely on these co-receptors to detect different chemicals. Through in vivo electrophysiology, we found that CO2 detection and inhibition in these neurons rely solely on Gr3, while Ir25a modulates the response to specific odors, indicating its role in fine-tuning odor detection.