Organization of the Escherichia coli and Salmonella typhimurium chromosomes between flagellar regions IIIa and IIIb, including a large non-coding region

Raha, Manidipa; Kihara, May; Kawagishi, Ikuro; Macnab, Robert M.

doi:10.1099/00221287-139-7-1401

Cited by 12 publications

(9 citation statements)

References 15 publications

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“…ORF gtgC is similar to ORFs found within a pathogenicity island‐associated prophage and in the adherence factor plasmid of enteropathogenic E. coli (Perna et al ., 1998; Tobe et al ., 1999). ORF gtgD shows identity to the yedK locus of E. coli (Raha et al ., 1993; Blattner et al ., 1997). Element e1 is a 35 bp sequence identical to S. typhimurium tRNA 2 Pro gene.…”

Section: Resultsmentioning

confidence: 99%

Variable assortment of prophages provides a transferable repertoire of pathogenic determinants in Salmonella

Figueroa‐Bossi

Uzzau

Maloriol

et al. 2001

Molecular Microbiology

269

253

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Gene transfer between separate lineages of a bacterial pathogen can promote recombinational divergence and the emergence of new pathogenic variants. Temperate bacteriophages, by virtue of their ability to carry foreign DNA, are potential key players in this process. Our previous work has shown that representative strains of Salmonella typhimurium (LT2, ATCC14028 and SL1344) are lysogenic for two temperate bacteriophages: Gifsy‐1 and Gifsy‐2. Several lines of evidence suggested that both elements carry genes that contribute to Salmonella virulence. One such gene, on the Gifsy‐2 prophage, codes for the [Cu, Zn] superoxide dismutase SodCI. Other putative pathogenicity determinants were uncovered more recently. These include genes for known or presumptive type III‐translocated proteins and a locus, duplicated on both prophages, showing sequence similarity to a gene involved in Salmonella enteropathogenesis (pipA). In addition to Gifsy‐1 and Gifsy‐2, each of the above strains was found to harbour a specific set of prophages also carrying putative pathogenicity determinants. A phage released from strain LT2 and identified as phage Fels‐1 carries the nanH gene and a novel sodC gene, which was named sodCIII. Strain ATCC14028 releases a lambdoid phage, named Gifsy‐3, which contains the phoP/phoQ‐activated pagJ gene and the gene for the secreted leucine‐rich repeat protein SspH1. Finally, a phage specifically released from strain SL1344 was identified as SopEΦ. Most phage‐associated loci transferred efficiently between Salmonella strains of the same or different serovars. Overall, these results suggest that lysogenic conversion is a major mechanism driving the evolution of Salmonella bacteria.

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Section: Resultsmentioning

confidence: 99%

Variable assortment of prophages provides a transferable repertoire of pathogenic determinants in Salmonella

Figueroa‐Bossi

Uzzau

Maloriol

et al. 2001

Molecular Microbiology

269

253

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“…1): it is the only gene in its transcriptional unit, it is divergent from the two other flagellar operons in its region (region IIIb), and it is located at one end of a large, mostly noncoding region between flagellar regions IIIa and IIIb (17,21). The former two characteristics are suggestive of a somewhat specialized function for the fliE gene product.…”

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confidence: 91%

Interaction between FliE and FlgB, a Proximal Rod Component of the Flagellar Basal Body of Salmonella

2000

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FliE is a flagellar basal body protein of Salmonella whose detailed location and function have not been established. A mutant allele of fliE, which caused extremely poor flagellation and swarming, generated extragenic suppressors, all of which mapped to flgB, one of four genes encoding the basal body rod; the fliE flgB pseudorevertants were better flagellated and swarmed better than the fliE parent, especially when the temperature was reduced from 37 to 30°C. Motility of the pseudorevertants in liquid culture was markedly better than motility on swarm plates; we interpret this to mean that reduced flagellation is less deleterious at low viscous loads. Overproduction of the mutant FliE protein improved the motility of the parental fliE mutant and its pseudorevertants, though not to wild-type levels. Overproduction of suppressor FlgB (but not wild-type FlgB) in the fliE mutant also resulted in improved motility. The second-site FlgB mutation by itself had no phenotype; cells swarmed as well as wild-type cells. When overproduced, wild-type FliE was dominant over FliE-V99G, but the reverse was not true; that is, overproduced FliE-V99G was not negatively dominant over wild-type FliE. We conclude that the mutant protein has reduced probability of assembly but, if assembled, functions relatively well. Export of the flagellar protein FlgD, which is known to be FliE dependent, was severely impaired by the FliE-V99G mutation but was significantly improved in the suppressor strains. The FliE mutation, V99G, was close to the C terminus of the 104-amino-acid sequence; the suppressing mutations in FlgB were all either G119E or G129D, close to the C terminus of its 138-amino-acid sequence. Affinity blotting experiments between FliE as probe and various basal body proteins as targets and vice versa revealed strong interactions between FliE and FlgB; much weaker interactions between FliE and other rod proteins were observed and probably derive from the known similarities among these proteins. We suggest that FliE subunits constitute a junction zone between the MS ring and the rod and also that the proximal rod structure consists of FlgB subunits.

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“…E. coli region III contains seven flagellar (fli) operons, which are separated into regions IIIa and IIIb by the large intervening segment that includes the amyA gene, a few open reading frames (ORF), and an NC region (Fig. 1B) (33,43,44 This laboratory…”

Section: Resultsmentioning

confidence: 99%

“…Most of the E. coli region III operons are cloned, and their restriction maps are reported (6,25,34,39,40,44). We have also isolated these operons as three clones, pAZY1, pECF181, and pEHR274 ( Fig.…”

Section: Methodsmentioning

confidence: 99%

“…1), which were constructed by ligating EcoRI fragments of W3110 DNA to the P lac promoter of pMW119 and which were able to confer motility on the E. coli fliA, fliC, and fliK mutants (Table 2), respectively. Each plasmid was mapped for various restriction sites, and fli genes were assigned to the map by making reference to the published data (6,25,34,40,44). Loci of fli genes were then confirmed by complementation with E. coli fli mutants after being subcloned.…”

Section: Methodsmentioning

confidence: 99%

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Cloning and characterization of the region III flagellar operons of the four Shigella subgroups: genetic defects that cause loss of flagella of Shigella boydii and Shigella sonnei

1997

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To detect genetic defects that might have caused loss of flagella in Shigella boydii and Shigella sonnei, the region III flagellar (fli) operons were cloned from certain strains and analyzed with reference to the restriction maps and genetic maps of Escherichia coli fli operons. S. boydii NCTC9733 (strain C5 in this paper) had the 988-bp internal deletion in the fliF gene that encodes a large substructural protein of the basal body. Two strains (C1 and C8) had deletions of the entire fliF operon, and the remaining three (C3, C4, and C9) differed in the size of the restriction fragments carrying the fliF and fliL operons. Loss of flagella in S. boydii appears to originate in some defect in the fliF operon. S. sonnei IID969 lacked the fliD gene and, in place of it, carried two IS600 elements as inverted repeats. Genes downstream from fliD were not detected in the cloned fragment despite its large size but did appear elsewhere in the chromosome. The fliD gene encodes a cap protein of the flagellar filament, and its deletion results in overexpression of class 3 operons by the increased amount of FliA ( F ) caused by the excess export of the anti-sigma factor FlgM. Three other strains also had the fliD deletion, and two of them had another deletion in the fliF-fliG-fliH region. The fliD deletion might be the primary cause of loss of flagella in S. sonnei. The lack of FliF or FliD in each subgroup is discussed in connection with the maintenance of virulence and bacterial growth. We also discuss the process of loss of flagella in relation to transposition of IS elements and alterations of the noncoding region, which were found to be common to at least three subgroups.The genus Shigella is divided into four subgroups or species: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei (46). All are pathogens which cause diarrhea and dysentery in humans and certain other primates (37). Shigellae have been regarded as nonmotile organisms lacking flagella (15), and this characteristic has been used as one of the taxonomic and diagnostic criteria to distinguish shigellae from other enteric bacteria. However, it has been reported that some prototypical strains of the four subgroups and two fresh clinical isolates of S. sonnei are sparsely flagellate (19). We have not yet detected any motile strain among the four subgroups in the more than 20 laboratory strains we have examined so far; instead we have detected defective flagellar genes in some strains of these subgroups (4, 56). Therefore, we have been studying loss of motility by shigellae from the point of view that almost all shigellae are nonmotile because of a lack of flagellation.Approximately 50 genes, composing at least 13 operons, are involved in the biogenesis and functioning of a flagellum of Escherichia coli and Salmonella typhimurium (33). These operons are clustered into three different regions on the chromosome. Region I operons mainly contain flagellar structural genes designated flg; region II contains a mixture of flagellar (flh) and mot...

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Organization of the Escherichia coli and Salmonella typhimurium chromosomes between flagellar regions IIIa and IIIb, including a large non-coding region

Cited by 12 publications

References 15 publications

Variable assortment of prophages provides a transferable repertoire of pathogenic determinants in Salmonella

Variable assortment of prophages provides a transferable repertoire of pathogenic determinants in Salmonella

Interaction between FliE and FlgB, a Proximal Rod Component of the Flagellar Basal Body of Salmonella

Cloning and characterization of the region III flagellar operons of the four Shigella subgroups: genetic defects that cause loss of flagella of Shigella boydii and Shigella sonnei

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