Taste-2 receptors (TAS2Rs), which belong to the G-protein coupled receptor (GPCR) family, are receptors for bitter taste perception. The aim of this study was to investigate whether zinc deficiency affects the expression of TAS2R genes. The promoter activity of the TAS2R7, TAS2R8, and TAS2R42 genes were determined in Ca9-22 oral squamous cell carcinoma cells cultured in the presence or absence of zinc. Luciferase reporter assays showed that zinc deprivation inhibited TAS2R8 promoter activity, but not the promoter activity of the other two genes. Treatment of the cells with N,N,N’,N’-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine (TPEN), an intracellular chelator of Zn²⁺, in the presence of 10% fetal bovine serum reduced TAS2R8 promoter activity. Truncation/deletion mutants of TAS2R8 promoter-luciferase constructs showed that the region from nucleotide −1152 to nucleotide −925 was critical for intracellular zinc dependency and contained a CCCTC-binding factor (CTCF) binding motif. A chromatin immunoprecipitation (ChiP) assay showed that CTCF bound specifically to this region, a binding abrogated by zinc deficiency, suggesting that CTCF plays a critical role in zinc-dependent bitter taste perception through TAS2R8.

味道 2 受体 (TAS2R) 属于 G 蛋白偶联受体 (GPCR) 家族，是苦味感知的受体。本研究的目的是调查缺锌是否影响TAS2R基因的表达。TAS2R7、TAS2R8和TAS2R42基因的启动子活性在存在或不存在锌的情况下培养的Ca9-22口腔鳞状细胞癌细胞中测定。荧光素酶报告基因检测表明，缺锌会抑制TAS2R8启动子活性，但不会抑制其他两个基因的启动子活性。用N , N , N ', N处理细胞'-tetrakis(2-pyridinylmethyl)-1,2-乙二胺(TPEN)，一种Zn ²⁺的细胞内螯合剂，在10% 胎牛血清存在下降低了TAS2R8启动子活性。TAS2R8启动子-荧光素酶构建体的截断/缺失突变体表明，从核苷酸 -1152 到核苷酸 -925 的区域对于细胞内锌依赖性至关重要，并且含有 CCCTC 结合因子 (CTCF) 结合基序。染色质免疫沉淀 (ChiP) 测定表明 CTCF 与该区域特异性结合，这种结合因缺锌而取消，表明 CTCF 通过 TAS2R8 在锌依赖性苦味感知中起关键作用。