Hypermotility in Clostridium perfringens Strain SM101 Is Due to Spontaneous Mutations in Genes Linked to Cell Division

Abstract

Clostridium perfringens is a Gram-positive anaerobic pathogen of humans and animals. Although they lack flagella, C. perfringens bacteria can still migrate across surfaces using a type of gliding motility that involves the formation of filaments of bacteria lined up in an end-to-end conformation. In strain SM101, hypermotile variants are often found arising from the edges of colonies on agar plates. Hypermotile cells are longer than wild-type cells, and video microscopy of their gliding motility suggests that they form long, thin filaments that move rapidly away from a colony, analogously to swarmer cells in bacteria with flagella. To identify the cause(s) of the hypermotility phenotype, the genome sequences of normal strains and their direct hypermotile derivatives were determined and compared. Strains SM124 and SM127, hypermotile derivatives of strains SM101 and SM102, respectively, contained 10 and 6 single nucleotide polymorphisms (SNPs) relative to their parent strains. While SNPs were located in different genes in the two sets of strains, one feature in common was mutations in cell division genes, an ftsI homolog in strain SM124 (CPR_1831) and a minE homolog in strain SM127 (CPR_2104). Complementation of these mutations with wild-type copies of each gene restored the normal motility phenotype. A model explaining the principles underlying the hypermotility phenotype is presented.

Effects of Bile Acids and Nisin on the Production of Enterotoxin byClostridium perfringensin a Nutrient-Rich Medium

“…The total bacterial counts after 24 h of incubation were similar in cultures with and without additives, indicating that the concentrations of additives used were not inhibitory. Similar to the observation of Liu et al [ 34 ], C. perfringens SM101 had a long lag phase even while growing in BHI without bile acids and nisin ( Figure 2 and Supplementary Figure 2S ). The lag phase was longer than that observed for C. perfringens grown in fluid thioglycolate medium (FTH), which contains sodium thioglycolate and L-cysteine [ 21 ].…”

Regulation of the Min Cell Division Inhibition Complex by the Rcs Phosphorelay in Proteus mirabilis

“…In other bacteria, a minC mutation was found to reduce motility in Helicobacter pylori, but the mutant was highly elongated in liquid culture, which the authors hypothesized was the cause of reduced motility (35). In contrast, a mutation in a minE homolog in the Gram-positive bacterium Clostridium perfringens resulted in hypermotility and hyperelongation (36). In P. mirabilis, a null allele in minC, the proprietor of cell division inhibition in the Min system, did not induce hyperelongation in liquid culture or on solid surfaces in our study.…”