Mouslim C, Cano D A, Casadesús J
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Spain.
Mol Gen Genet. 1998 Jul;259(1):46-53. doi: 10.1007/s004380050787.
Two loci involved in the pleiotropic response of His(c) strains of Salmonella typhimurium (sfiX and sfiY) have been characterized at the molecular level. The sfiX gene (CS 44) has been identified as a homolog of the E. coli gene sanA, located downstream of the cytidine deaminase gene (cdd). The cdd-sanA (or cdd-sfiX) operon shows a highly conserved structure in E. coli and Salmonella. Like its E. coli homolog, the sfiX gene of S. typhimurium is required for vancomycin resistance at high temperature. The dual effect of sfiX mutations (induction of vancomycin sensitivity and suppression of cell division inhibition) suggests a link between SfiX function and murein synthesis. The sfiY locus (CS 85), contains two genes arranged in a single transcriptional unit. The upstream gene is a homolog of the E. coli gene rfe; mutations in this gene suppress the cell division defect of His(c) strains. The suppressor effect of rfe mutations can be reproduced by tunicamycin, suggesting that suppression of filamentation results from an increase in the intracellular concentration of UDP-N-acetyl-D-glucosamine. The gene located downstream of rfe is also found in E. coli but its function is unknown. Insertions in rfe suppress the methionine requirement of His(c) strains of S. typhimurium by a polar effect on the downstream gene, tentatively designated metN. Complementation with a rfe+ clone indicates that the rfe gene is not involved in the methionine requirement of His(c) strains. Thus metN expression appears to cause methionine auxotrophy in a His(c) background.
参与鼠伤寒沙门氏菌His(c)菌株多效性反应的两个基因座（sfiX和sfiY）已在分子水平上得到表征。sfiX基因（CS 44）已被鉴定为大肠杆菌基因sanA的同源物，位于胞苷脱氨酶基因（cdd）的下游。cdd-sanA（或cdd-sfiX）操纵子在大肠杆菌和沙门氏菌中显示出高度保守的结构。与它的大肠杆菌同源物一样，鼠伤寒沙门氏菌的sfiX基因在高温下对万古霉素耐药性是必需的。sfiX突变的双重作用（诱导万古霉素敏感性和抑制细胞分裂抑制）表明SfiX功能与胞壁质合成之间存在联系。sfiY基因座（CS 85）包含两个以单一转录单元排列的基因。上游基因是大肠杆菌基因rfe的同源物；该基因中的突变可抑制His(c)菌株的细胞分裂缺陷。rfe突变的抑制作用可以通过衣霉素重现，这表明丝状化的抑制是由于UDP-N-乙酰-D-葡萄糖胺细胞内浓度的增加。rfe下游的基因在大肠杆菌中也有发现，但其功能未知。rfe中的插入通过对下游基因（暂时命名为metN）的极性作用抑制了鼠伤寒沙门氏菌His(c)菌株对蛋氨酸的需求。用rfe+克隆进行互补表明rfe基因与His(c)菌株对蛋氨酸的需求无关。因此，metN的表达似乎在His(c)背景下导致蛋氨酸营养缺陷。
