Abstract
Anthrax toxins and capsules, which are encoded by genes located on pXO1 and pXO2, respectively, are major virulence factors of Bacillus anthracis. Our previous studies demonstrated that exposure to high-temperatures is unable to abolish the pXO1 plasmid of the Pasteur II strain, but the growth of the strain was obviously slower than that of the Sterne strain and wild-type virulent strain. To elucidate a potential regulatory mechanism of slowing growth, we employed comparative genome and bioinformatic analysis and revealed a unique SNP (G to T) at the 143135 bp position in pXO1 that is possibly involved in the mediation of growth of Pasteur II. However, the T to G mutation in groR did not result in any change of the amino acid sequence. A predominant nucleotide G existed at the 143135 bp in pXO1 of 100 wild-type B. anthracis isolates and 9 isolates documented in GenBank, whereas T replaced G in pXO1 of the Pasteur II strain. Further analysis indicate that the SNP is located in a gene between 143042 and 143173 bp, and that it encodes a small protein of 43 amino acids and is termed as a growth regulator (GroR). Site-directed mutagenesis and gene deletion demonstrates that groR regulates the growth and spore formation of B. anthracis. Our results indicate that the pXO1 plasmid is involved in the regulation of growth and spore formation in B. anthracis.
Highlights
Bacillus anthracis is a spore-forming, gram-positive bacterium and it exists as dormant spores in the environment
The results showed that nucleotide G, at the corresponding position of Pasteur II, was present in all tested wild-type strains, whereas nucleotide T was only present in the Pasteur II strain (Figure 1A)
Further analysis revealed that the Single Nucleotide Polymorphisms (SNPs) was located in an open reading frame that encodes a small protein composed of 43 amino acids, which was designated as a growth regulator
Summary
Bacillus anthracis is a spore-forming, gram-positive bacterium and it exists as dormant spores in the environment. When the spores enter a mammalian host through a cutaneous injury, gastrointestinal ingestion or inhalation, the bacteria rapidly proliferate and produce anthrax toxins and capsule (Liang, 1995). The anthrax toxins are encoded by cya, lef, and pagA genes, which are located in a pathogenicity island of pXO1 (Mikesell et al, 1983; Okinaka et al, 1999). SNP’s Regulation of B. anthracis Phenotypes upon transition of the pathogen from the external environment to the host (Ezzell and Abshire, 1988; Bartkus and Leppla, 1989; Koehler et al, 1994; Sirard et al, 1994). The poly-r-D-glutamic acid capsule is synthesized by the capBCADE operon located on pXO2 (Uchida et al, 1986; Makino et al, 1989)
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