Aakra Agot, Vebø Heidi, Indahl Ulf, Snipen Lars, Gjerstad Oystein, Lunde Merete, Nes Ingolf F
Department of Chemistry, Biotechnology and Food Science, The Norwegian University of Life Sciences, P.O. Box 5003, 1432 As, Norway.
Int J Microbiol. 2010;2010:483048. doi: 10.1155/2010/483048. Epub 2010 Jun 15.
Many Enterococcus faecalis strains display tolerance or resistance to many antibiotics, but genes that contribute to the resistance cannot be specified. The multiresistant E. faecalis V583, for which the complete genome sequence is available, survives and grows in media containing relatively high levels of chloramphenicol. No specific genes coding for chloramphenicol resistance has been recognized in V583. We used microarrays to identify genes and mechanisms behind the tolerance to chloramphenicol in V583, by comparison of cells treated with subinhibitory concentrations of chloramphenicol and untreated V583 cells. During a time course experiment, more than 600 genes were significantly differentially transcribed. Since chloramphenicol affects protein synthesis in bacteria, many genes involved in protein synthesis, for example, genes for ribosomal proteins, were induced. Genes involved in amino acid biosynthesis, for example, genes for tRNA synthetases and energy metabolism were downregulated, mainly. Among the upregulated genes were EF1732 and EF1733, which code for potential chloramphenicol transporters. Efflux of drug out of the cells may be one mechanism used by V583 to overcome the effect of chloramphenicol.
许多粪肠球菌菌株对多种抗生素表现出耐受性或抗性，但导致这种抗性的基因尚不明确。具有完整基因组序列的多重耐药粪肠球菌V583能在含有较高浓度氯霉素的培养基中存活和生长。在V583中尚未识别出编码氯霉素抗性的特定基因。我们通过比较用亚抑制浓度氯霉素处理的细胞和未处理的V583细胞，利用微阵列来鉴定V583中对氯霉素耐受性背后的基因和机制。在一个时间进程实验中，超过600个基因发生了显著的差异转录。由于氯霉素会影响细菌中的蛋白质合成，许多参与蛋白质合成的基因，例如核糖体蛋白的基因，被诱导表达。主要下调的基因包括参与氨基酸生物合成的基因，例如tRNA合成酶的基因以及能量代谢相关基因。上调的基因中有EF1732和EF1733，它们编码潜在的氯霉素转运蛋白。药物从细胞中流出可能是V583用来克服氯霉素作用的一种机制。
