Ochs M, Veitinger S, Kim I, Welz D, Angerer A, Braun V
Universität Tübingen, Germany.
Mol Microbiol. 1995 Jan;15(1):119-32. doi: 10.1111/j.1365-2958.1995.tb02226.x.
Citrate-dependent Fe3+ transport into Escherichia coli K-12 is induced by iron and citrate. The inducer is probably ferric dicitrate which does not have to be taken up into the cytoplasm to induce transcription of the fec transport genes. Two regulatory genes, fecI and fecR, located upstream of the fecABCDE transport genes, are required for induction. We report that in vivo the chromosomally encoded FecI protein activates transcription of the fecA and fecB transport genes in response to ferric citrate and the FecR protein. Cells expressing chromosomally and plasmid-encoded truncated FecR derivatives no longer responded to ferric citrate and expressed the fec transport genes constitutively. The smallest active FecR derivative contained 59 amino acid residues as compared to the 317 residues of wild-type FecR. Constitutive induction was lower than induction of the FecR wild-type strain by ferric citrate. It is concluded that the N-terminal portion of FecR activates FecI and that the C-terminal portion of FecR responds to ferric citrate. Transcription of the fec transport genes is positively regulated by FecI and FecR and negatively regulated by the Fe2(+)-Fur repressor. Transcription activation and repression may occur independently of each other.
铁和柠檬酸盐可诱导柠檬酸依赖的Fe3+转运进入大肠杆菌K-12。诱导剂可能是柠檬酸铁，它不必进入细胞质就能诱导fec转运基因的转录。位于fecABCDE转运基因上游的两个调控基因fecI和fecR是诱导所必需的。我们报道，在体内，染色体编码的FecI蛋白响应柠檬酸铁和FecR蛋白激活fecA和fecB转运基因的转录。表达染色体和质粒编码的截短FecR衍生物的细胞不再对柠檬酸铁作出反应，并组成性地表达fec转运基因。与野生型FecR的317个氨基酸残基相比，最小的活性FecR衍生物含有59个氨基酸残基。组成性诱导低于柠檬酸铁对FecR野生型菌株的诱导。得出的结论是，FecR的N端部分激活FecI，而FecR的C端部分响应柠檬酸铁。fec转运基因的转录受FecI和FecR的正调控，受Fe2(+)-Fur阻遏物的负调控。转录激活和抑制可能相互独立发生。
