Centre for Biomedical Sciences, School of Biological Sciences, Royal Holloway University of London, Egham TW20 0EX, UK.
J Cell Sci. 2013 Dec 1;126(Pt 23):5465-76. doi: 10.1242/jcs.136440. Epub 2013 Sep 4.
Detection of substances tasting bitter to humans occurs in diverse organisms including the social amoeba Dictyostelium discoideum. To establish a molecular mechanism for bitter tastant detection in Dictyostelium, we screened a mutant library for resistance to a commonly used bitter standard, phenylthiourea. This approach identified a G-protein-coupled receptor mutant, grlJ(-), which showed a significantly increased tolerance to phenylthiourea in growth, survival and movement. This mutant was not resistant to a structurally dissimilar potent bitter tastant, denatonium benzoate, suggesting it is not a target for at least one other bitter tastant. Analysis of the cell-signalling pathway involved in the detection of phenylthiourea showed dependence upon heterotrimeric G protein and phosphatidylinositol 3-kinase activity, suggesting that this signalling pathway is responsible for the cellular effects of phenylthiourea. This is further supported by a phenylthiourea-dependent block in the transient cAMP-induced production of phosphatidylinositol (3,4,5)-trisphosphate (PIP3) in wild-type but not grlJ(-) cells. Finally, we have identified an uncharacterized human protein γ-aminobutyric acid (GABA) type B receptor subunit 1 isoform with weak homology to GrlJ that restored grlJ(-) sensitivity to phenylthiourea in cell movement and PIP3 regulation. Our results thus identify a novel pathway for the detection of the standard bitter tastant phenylthiourea in Dictyostelium and implicate a poorly characterized human protein in phenylthiourea-dependent cell responses.
检测人类感知苦味的物质存在于多种生物中,包括社会性阿米巴虫 Dictyostelium discoideum。为了建立 Dictyostelium 苦味感受体检测的分子机制,我们筛选了一个对常用苦味标准品苯硫脲具有抗性的突变体文库。这种方法鉴定了一个 G 蛋白偶联受体突变体 grlJ(-),其在生长、存活和运动方面对苯硫脲的耐受性显著增加。该突变体对结构上不相似的强苦味物质苯甲地那铵没有抗性,表明它不是至少另一种苦味物质的靶标。对参与苯硫脲检测的细胞信号通路的分析表明,该通路依赖于异三聚体 G 蛋白和磷脂酰肌醇 3-激酶活性,表明该信号通路负责苯硫脲的细胞效应。这进一步得到了苯硫脲依赖性阻断野生型细胞中短暂 cAMP 诱导的磷脂酰肌醇(3,4,5)-三磷酸(PIP3)产生的支持,但 grlJ(-) 细胞则没有。最后,我们鉴定了一个未表征的人类蛋白 γ-氨基丁酸(GABA)B 型受体亚基 1 异构体,与 GrlJ 具有微弱同源性,它恢复了 grlJ(-) 对细胞运动和 PIP3 调节中苯硫脲的敏感性。因此,我们的研究结果鉴定了一种在 Dictyostelium 中检测标准苦味物质苯硫脲的新途径,并暗示了一种在苯硫脲依赖性细胞反应中未被充分表征的人类蛋白的参与。