1887

Abstract

The Gram-negative pathogen strain M2 was found to exhibit a robust surface motility on low-percentage (0.2–0.4 %) agar plates. These patterns of motility were dramatically different depending on whether Difco or Eiken agar was used. Motility was observed in many, but not all, clinical and environmental isolates. The use of drop collapse assays to demonstrate surfactant production was unsuccessful, and the role of surfactants in M2 motility remains unclear. Surface motility was impaired by an insertion in , encoding a gene product that is often required for retraction of the type IV pilus. Motility was also dependent on quorum sensing, as a null allele in the autoinducer synthase decreased motility, and the addition of exogenous -(3-hydroxy)-dodecanoylhomoserine lactone (3-OH C-HSL) restored motility to the mutant. Transposon mutagenesis was used to identify additional genes required for motility and revealed loci encoding various functions: non-ribosomal synthesis of a putative lipopeptide, a sensor kinase (BfmS), a lytic transglycosylase, O-antigen biosynthesis (RmlB), an outer membrane porin (OmpA) and purine biosynthesis (PurK). Two of the above genes required for motility were highly activated by quorum sensing, and may explain, in part, the requirement for quorum sensing in motility.

Funding
This study was supported by the:
  • Atlanta Research and Education Foundation
  • National Institutes of Health (Award R01AI072219-01A1))
  • Department of Veterans Affairs
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2011-09-01
2021-10-27
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