Contribution of the Shigella flexneri Sit, Iuc, and Feo iron acquisition systems to iron acquisition in vitro and in cultured cells

被引:117
作者
Runyen-Janecky, LJ
Reeves, SA
Gonzales, EG
Payne, SM [1 ]
机构
[1] Univ Texas, Sect Mol Genet & Microbiol, Austin, TX 78712 USA
[2] Univ Texas, Inst Cellular & Mol Biol, Austin, TX 78712 USA
关键词
D O I
10.1128/IAI.71.4.1919-1928.2003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Shigella flexneri possesses multiple iron acquisition systems, including proteins involved in the synthesis and uptake of siderophores and the Feo system for ferrous iron utilization. We identified an additional S. flexneri putative iron transport gene, sitA, in a screen for S. flexneri genes that are induced in the eukaryotic intracellular environment. sitA was present in all Shigella species and in most enteroinvasive Escherichia coli strains but not in any other E. coli isolates tested. The sit locus consists of four genes encoding a potential ABC transport system. The deduced amino acid sequence of the S. flexneri sit locus was homologous to the Salmonella enterica serovar Typhimurium Sit and Yersinia pestis Yfe systems, which mediate both manganese and iron transport. The S. flexneri sit promoter was repressed by either iron or manganese, and the iron repression was partially dependent upon Fur. A sitA::cam mutation was constructed in S. flexneri. The sitA mutant showed reduced growth, relative to the wild type, in Luria broth containing an iron chelator but formed wild-type plaques on Henle cell monolayers, indicating that the sitA mutant was able to acquire iron and/or manganese in the host cell. However, mutants defective in two of these iron acquisition systems (sitA iucD, sitA feoB, and feoB iucD) formed slightly smaller plaques on Henle cell monolayers. A strain carrying mutations in sitA, feoB, and iucD did not form plaques on Henle cell monolayers.
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页码:1919 / 1928
页数:10
相关论文
共 56 条
[1]   Low iron availability modulates the course of Chlamydia pneumoniae infection [J].
Al-Younes, HM ;
Rudel, T ;
Brinkmann, V ;
Szczepek, AJ ;
Meyer, TF .
CELLULAR MICROBIOLOGY, 2001, 3 (06) :427-437
[2]   The Yfe system of Yersinia pestis transports iron and manganese and is required for full virulence of plague [J].
Bearden, SW ;
Perry, RD .
MOLECULAR MICROBIOLOGY, 1999, 32 (02) :403-414
[3]   An ABC transporter system of Yersinia pestis allows utilization of chelated iron by Escherichia coli SAB11 [J].
Bearden, SW ;
Staggs, TM ;
Perry, RD .
JOURNAL OF BACTERIOLOGY, 1998, 180 (05) :1135-1147
[4]  
Clarke Teresa E., 2001, Current Topics in Medicinal Chemistry, V1, P7, DOI 10.2174/1568026013395623
[5]   MOLECULAR-CLONING OF THE FERRICHROME-IRON RECEPTOR OF ESCHERICHIA-COLI K-12 [J].
COULTON, JW ;
MASON, P ;
DUBOW, MS .
JOURNAL OF BACTERIOLOGY, 1983, 156 (03) :1315-1321
[6]   IRON UPTAKE IN PLESIOMONAS-SHIGELLOIDES - CLONING OF THE GENES FOR THE HEME-IRON UPTAKE SYSTEM [J].
DASKALEROS, PA ;
STOEBNER, JA ;
PAYNE, SM .
INFECTION AND IMMUNITY, 1991, 59 (08) :2706-2711
[7]   CONGO RED BINDING PHENOTYPE IS ASSOCIATED WITH HEMIN BINDING AND INCREASED INFECTIVITY OF SHIGELLA-FLEXNERI IN THE HELA-CELL MODEL [J].
DASKALEROS, PA ;
PAYNE, SM .
INFECTION AND IMMUNITY, 1987, 55 (06) :1393-1398
[8]   TRANSFERRIN, IRON, AND SERUM-LIPIDS ENHANCE OR INHIBIT MYCOBACTERIUM-AVIUM REPLICATION IN HUMAN MACROPHAGES [J].
DOUVAS, GS ;
MAY, MH ;
CROWLE, AJ .
JOURNAL OF INFECTIOUS DISEASES, 1993, 167 (04) :857-864
[9]   Opening the iron box:: Transcriptional metalloregulation by the fur protein [J].
Escolar, L ;
Pérez-Martín, J ;
De Lorenzo, V .
JOURNAL OF BACTERIOLOGY, 1999, 181 (20) :6223-6229
[10]   CONSTRUCTION OF A BROAD HOST RANGE COSMID CLONING VECTOR AND ITS USE IN THE GENETIC-ANALYSIS OF RHIZOBIUM MUTANTS [J].
FRIEDMAN, AM ;
LONG, SR ;
BROWN, SE ;
BUIKEMA, WJ ;
AUSUBEL, FM .
GENE, 1982, 18 (03) :289-296