Abstract
Strains in the genus Shigella are nonmotile, but they retain some cryptic flagellar operons whether functional or defective (A. Tominaga, M. A.-H. Mahmoud, T. Mukaihara, and M. Enomoto, Mol. Microbiol. 12:277-285, 1994). To disclose the cause of motility loss in shigellae, the presence or defectiveness of the flhD and flhC genes, composing the master operon whose mutation causes inactivation of the entire flagellar regulon, was examined in the four Shigella subgroups. The flhD operon cloned from Shigella boydii and Shigella sonnei can activate, though insufficiently, the regulon in the Escherichia coli flhD or flhC mutant background. The clone from Shigella dysenteriae has a functional flhD gene and nonfunctional flhC gene, and its inactivation has been caused by the IS1 element inserted in its 5' end. The operon of Shigella flexneri is nonfunctional and has suffered an IS1- insertion mutation at the 5' end of the flhD gene. Comparison of restriction maps indicates that only the central 1.8-kb region, including part of the flhC gene and its adjacent mot operon, is conserved among the four Shigella subgroups as well as in E. coli, but in Salmonella typhimurium the whole map is quite different from the others. Motility loss in shigellae is not attributable to genetic damage in the master operon of a common ancestor, but it occurs separately in respective ancestors of the four subgroups, and in both S. dysenteriae and S. flexneri IS1 insertion in the master operon might he the primary cause of motility loss.
| Original language | English |
|---|---|
| Pages (from-to) | 3722-3726 |
| Number of pages | 5 |
| Journal | Journal of Bacteriology |
| Volume | 178 |
| Issue number | 13 |
| Publication status | Published - 1996 |
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ASJC Scopus subject areas
- Applied Microbiology and Biotechnology
- Immunology
Cite this
Detection and characterization of the flagellar master operon in the four Shigella subgroups. / Al Mamun, Abu Amar M; Tominaga, Akira; Enomoto, Masatoshi.
In: Journal of Bacteriology, Vol. 178, No. 13, 1996, p. 3722-3726.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Detection and characterization of the flagellar master operon in the four Shigella subgroups
AU - Al Mamun, Abu Amar M
AU - Tominaga, Akira
AU - Enomoto, Masatoshi
PY - 1996
Y1 - 1996
N2 - Strains in the genus Shigella are nonmotile, but they retain some cryptic flagellar operons whether functional or defective (A. Tominaga, M. A.-H. Mahmoud, T. Mukaihara, and M. Enomoto, Mol. Microbiol. 12:277-285, 1994). To disclose the cause of motility loss in shigellae, the presence or defectiveness of the flhD and flhC genes, composing the master operon whose mutation causes inactivation of the entire flagellar regulon, was examined in the four Shigella subgroups. The flhD operon cloned from Shigella boydii and Shigella sonnei can activate, though insufficiently, the regulon in the Escherichia coli flhD or flhC mutant background. The clone from Shigella dysenteriae has a functional flhD gene and nonfunctional flhC gene, and its inactivation has been caused by the IS1 element inserted in its 5' end. The operon of Shigella flexneri is nonfunctional and has suffered an IS1- insertion mutation at the 5' end of the flhD gene. Comparison of restriction maps indicates that only the central 1.8-kb region, including part of the flhC gene and its adjacent mot operon, is conserved among the four Shigella subgroups as well as in E. coli, but in Salmonella typhimurium the whole map is quite different from the others. Motility loss in shigellae is not attributable to genetic damage in the master operon of a common ancestor, but it occurs separately in respective ancestors of the four subgroups, and in both S. dysenteriae and S. flexneri IS1 insertion in the master operon might he the primary cause of motility loss.
AB - Strains in the genus Shigella are nonmotile, but they retain some cryptic flagellar operons whether functional or defective (A. Tominaga, M. A.-H. Mahmoud, T. Mukaihara, and M. Enomoto, Mol. Microbiol. 12:277-285, 1994). To disclose the cause of motility loss in shigellae, the presence or defectiveness of the flhD and flhC genes, composing the master operon whose mutation causes inactivation of the entire flagellar regulon, was examined in the four Shigella subgroups. The flhD operon cloned from Shigella boydii and Shigella sonnei can activate, though insufficiently, the regulon in the Escherichia coli flhD or flhC mutant background. The clone from Shigella dysenteriae has a functional flhD gene and nonfunctional flhC gene, and its inactivation has been caused by the IS1 element inserted in its 5' end. The operon of Shigella flexneri is nonfunctional and has suffered an IS1- insertion mutation at the 5' end of the flhD gene. Comparison of restriction maps indicates that only the central 1.8-kb region, including part of the flhC gene and its adjacent mot operon, is conserved among the four Shigella subgroups as well as in E. coli, but in Salmonella typhimurium the whole map is quite different from the others. Motility loss in shigellae is not attributable to genetic damage in the master operon of a common ancestor, but it occurs separately in respective ancestors of the four subgroups, and in both S. dysenteriae and S. flexneri IS1 insertion in the master operon might he the primary cause of motility loss.
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M3 - Article
C2 - 8682772
AN - SCOPUS:0029884412
VL - 178
SP - 3722
EP - 3726
JO - Journal of Bacteriology
JF - Journal of Bacteriology
SN - 0021-9193
IS - 13
ER -