A study showed that the expression of Tas2r genes was significantly upregulated in an inflammation model mimicking bacterial infection, leading to increased neural and behavioral responses to bitter compounds in mice. Single-cell ATAC-seq experiments also revealed cell-type specific chromatin accessibility of Tas2r genes, which was further enhanced by lipopolysaccharide.
T2R bitter receptors, encoded by Tas2r genes, are not only critical for bitter taste signal transduction but also important for defense against bacteria and parasites. However, little is known about whether and how Tas2r gene expression are regu-lated. Here, we show that in an inflammation model mimicking bacterial infection using lipopolysaccharide, the expression of many Tas2rs was significantly upregu-lated and mice displayed markedly increased neural and behavioral responses to bitter compounds. Using single-cell assays for transposase-accessible chromatin with sequencing (scATAC-seq), we found that the chromatin accessibility of Tas2rs was highly celltype specific and lipopolysaccharide increased the accessi-bility of many Tas2rs. scATAC-seq also revealed substantial chromatin remodel-ing in immune response genes in taste tissue stem cells, suggesting potential long-lasting effects. Together, our results suggest an epigenetic mechanism con-necting inflammation, Tas2r gene regulation, and altered bitter taste, which may explain heightened bitter taste that can occur with infections and cancer treatments.
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