Department of Biochemistry and Molecular Biology, Faculty of Agriculture and Bioscience, Hirosaki University, Bunkyo-cho 3, Hirosaki, Aomori 036-8561, Japan.
J Biochem. 2021 Apr 29;169(4):485-489. doi: 10.1093/jb/mvaa122.
Deleting the gene for small RNA GcvB in Escherichia coli was found to increase the sensitivity to several aminoglycoside antibiotics, such as neomycin, streptomycin, kanamycin, kasugamycin and spectinomycin, at low concentrations. GcvB, conserved in gram-negative enteric bacteria, is known to negatively control the expression of many genes for amino acid incorporation systems, especially the periplasmic ABC-transporter proteins. Deletions of several amino acid transporter genes in ΔgcvB cells decreased the antibiotic sensitivity to the wild-type level, suggesting that those genes are involved in uptake of aminoglycosides into the cell. Since GcvB is constitutively synthesized in growing cells, repressing synthesis of amino acid transporters, it contributes to the intrinsic resistance to several aminoglycoside antibiotics.
在大肠杆菌中删除小 RNA GcvB 的基因被发现会增加对几种氨基糖苷类抗生素的敏感性，如低浓度的新霉素、链霉素、卡那霉素、井冈霉素和壮观霉素。GcvB 在革兰氏阴性肠道细菌中保守，已知它负调控许多氨基酸摄取系统基因的表达，特别是周质 ABC 转运蛋白。ΔgcvB 细胞中几种氨基酸转运基因的缺失降低了抗生素对野生型的敏感性，表明这些基因参与了氨基糖苷类抗生素进入细胞的摄取。由于 GcvB 在生长细胞中持续合成，抑制氨基酸转运体的合成，因此它有助于对几种氨基糖苷类抗生素的固有耐药性。
