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 be the primary cause of motility loss.