ArticleMolecular microbiology2016
The roles of AtxA orthologs in virulence of anthrax-like Bacillus cereus G9241.
Article in Molecular microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Review
- PRD-Containing Virulence Regulators (PCVRs) in Pathogenic Bacteria.Frontiers in cellular and infection microbiology · 2021Review
- You Can'tFrontiers in microbiology · 2020Review
- TheMicrobiology spectrum · 2019Review
- Certhrax Is an Antivirulence Factor for the Anthrax-Like Organism Bacillus cereus Strain G9241.Infection and immunity · 2018Article
- Expression and contribution to virulence of each polysaccharide capsule of Bacillus cereus strain G9241.PloS one · 2018Article
- Assembly and Function of the Bacillus anthracis S-Layer.Annual review of microbiology · 2017Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
AtxA is a critical transcriptional regulator of plasmid-encoded virulence genes in Bacillus anthracis. Bacillus cereus G9241, which caused an anthrax-like infection, has two virulence plasmids, pBCXO1 and pBC210, that each harbor toxin genes and a capsule locus. G9241 also produces two orthologs of AtxA: AtxA1, encoded on pBCXO1, and AtxA2, encoded on pBC210. The amino acid sequence of AtxA1 is identical to that of AtxA from B. anthracis, while the sequences of AtxA1 and AtxA2 are 79% identical and 91% similar to one another. We found by qRT-PCR that AtxA1 and AtxA2 function as positive regulators of toxin (AtxA1) and capsule operon (both) transcription in G9241 and that a ΔatxA1 mutant produced lower levels of the anthrax toxins and no hyaluronic acid capsule. Deletion of atxA1 or atxA2 decreased the virulence of spores administered intranasally or subcutaneously to C57BL/6 mice but not to A/J mice, and deletion of both genes rendered spores avirulent in A/J mice. In addition, unlike AtxA1, AtxA2 did not form stable homomultimers in vitro, although AtxA1 and AtxA2 formed heterodimers. Our data show that AtxA1 is the primary regulator of G9241 virulence factor expression and that AtxA1 and AtxA2 are both required for full virulence.
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