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A plasmid-encoded papB paralogue modulates autoaggregation of Escherichia coli transconjugants

Rubén Monárrez1, Iruka N Okeke2,3

  • 1Department of Biology, Haverford College, Haverford, Pennsylvania, USA.

BMC Research Notes
|December 15, 2020
PubMed
Abstract

Insights

A plasmid region deletion caused bacterial hyper-autoaggregation. A papB/pefB-like gene was identified as responsible for down-regulating host adhesins, impacting bacterial colonization and transfer.

Area of Science:

  • Microbiology
  • Bacterial genetics
  • Antimicrobial resistance

Background:

  • Plasmids facilitate antimicrobial resistance transmission in enteric bacteria.
  • Plasmids confer selective advantages beyond resistance genes.
  • A specific plasmid (pMB2) deletion induced hyper-autoaggregation in Escherichia coli.

Purpose of the Study:

  • To determine the genetic basis of hyper-autoaggregation caused by a pMB2-derived mini-plasmid.
  • To identify genes responsible for altered bacterial phenotypes.
  • To understand plasmid-mediated effects on bacterial behavior.

Main Methods:

  • Deletion of a 32 Kb fitness-conferring region from the pMB2 plasmid.
  • Cloning and expression of a papB/pefB-like gene.
  • Phenotypic analysis of Escherichia coli strains in fim-negative backgrounds.

Main Results:

  • The deleted fragment contained nutrient acquisition genes, transposases, integrases, and a papB/pefB-like gene.
  • The cloned papB/pefB paralogue reduced the hyper-autoaggregation phenotype.
  • Hyper-autoaggregation was dependent on the fim gene, indicating regulation of host adhesins.

Conclusions:

  • A novel gene (papB/pefB paralogue) was identified that down-regulates host adhesins.
  • Trans-acting papB/pefB paralogues can function outside adhesin clusters.
  • Plasmid modification of bacterial colonization may enhance horizontal gene transfer.
Keywords:
AutoaggregationFimbrial regulationPapBPefBPlasmid

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