Genes governing swarming in Bacillus subtilis and evidence for a phase variation mechanism controlling surface motility

• Published in: Molecular microbiology Vol. 52; no. 2; pp. 357 - 369
• Main Authors: Kearns, Daniel B., Chu, Frances, Rudner, Rivka, Losick, Richard
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.04.2004; Blackwell Science; Blackwell Publishing Ltd
• Subjects: Amino Acid Sequence; Anti-Bacterial Agents - pharmacology; Bacillus subtilis; Bacillus subtilis - genetics; Bacillus subtilis - physiology; Bacillus subtilis - ultrastructure; Base Sequence; Biological and medical sciences; DNA Transposable Elements; Flagella - physiology; Frameshift Mutation; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Bacterial; Genes, Bacterial; Genetic Variation; Lipopeptides; Microbiology; Molecular Sequence Data; Movement; Mutagenesis, Insertional; Open Reading Frames; Peptides, Cyclic - pharmacology; Motility; Bacillales; Gene; Microbiology; Bacillus subtilis; Bacteria; Bacillaceae
• ISSN: 0950-382X; 1365-2958; 1365-2958
• DOI: 10.1111/j.1365-2958.2004.03996.x

Summary Undomesticated strains of Bacillus subtilis, but not laboratory strains, exhibit robust swarming motility on solid surfaces. The failure of laboratory strains to swarm is caused by a mutation in a gene (sfp) needed for surfactin synthesis and a mutation(s) in an additional unknown gene(s). Insertional mutagenesis of the undomesticated 3610 strain with the transposon mini‐Tn10 was carried out to discover genes needed for swarming but not swimming motility. Four such newly identified swarming genes are reported, three of which (swrA, swrB, and efp) had not been previously characterized and one of which (swrC) was known to play a role in resistance to the antibacterial effect of surfactin. Laboratory strains were found to harbour a frameshift mutation in the swrA gene. When corrected for the swrA mutation, as well as the mutation in sfp, laboratory strains regained the capacity to swarm and did so as robustly as the wild strain. The swrA mutation was an insertion of an A:T base pair in a homopolymeric stretch of eight A:T base pairs, and readily reverted to the wild type. These findings suggest that the swrA insertion and its reversion take place by slipped‐strand mispairing during DNA replication and that swarming motility is subject to phase variation.