Munson Amanda M, Love Sherie L, Shu Jianfen, Palanivel Vikram R, Rosenwald Anne G
Department of Biology, Georgetown University, Washington, DC 20057, USA.
Biochem Biophys Res Commun. 2004 Mar 12;315(3):617-23. doi: 10.1016/j.bbrc.2004.01.099.
ATC1/LIC4, previously identified as a suppressor of the Li(+)-sensitive phenotype of calcineurin mutants, was also identified as a suppressor of the hygromycin B-sensitive phenotype of strains lacking the G protein gene, ARL1. Although loss of ARL1 confers several phenotypes, including sensitivity to hygromycin B and Li(+), reduced influx of K(+), and increased secretion of carboxypeptidase Y (CPY), loss of ATC1 was without effect by these and other measures. However, loss of ATC1 in an arl1 background exacerbated ion sensitivities, although not the CPY phenotype. Moreover, overexpression of ATC1 in an arl1 background partially suppressed ion sensitivities, but not the CPY phenotype. Additionally, expression of ENA1, the Na(+)/Li(+) efflux ATPase, and activated calcineurin, but not normal calcineurin, suppressed the Li(+)-sensitive phenotype of the arl1 atc1 double mutant. These results show ARL1 and ATC1 interact to control intracellular ion levels, but ATC1 has little influence on other functions of ARL1.
ATC1/LIC4，先前被鉴定为钙调神经磷酸酶突变体锂敏感表型的抑制因子，也被鉴定为缺乏G蛋白基因ARL1的菌株潮霉素B敏感表型的抑制因子。尽管ARL1的缺失会导致多种表型，包括对潮霉素B和锂敏感、钾离子内流减少以及羧肽酶Y（CPY）分泌增加，但ATC1的缺失在这些及其他指标上并无影响。然而，在arl1背景下ATC1的缺失加剧了离子敏感性，尽管对CPY表型没有影响。此外，在arl1背景下ATC1的过表达部分抑制了离子敏感性，但对CPY表型没有抑制作用。另外，钠/锂外流ATP酶ENA1的表达以及活化的钙调神经磷酸酶，而非正常的钙调神经磷酸酶，抑制了arl1 atc1双突变体的锂敏感表型。这些结果表明ARL1和ATC1相互作用以控制细胞内离子水平，但ATC1对ARL1的其他功能影响很小。
