A plasmid-encoded papB paralogue modulates autoaggregation of Escherichia coli transconjugants
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RESEARCH NOTE
A plasmid‑encoded papB paralogue modulates autoaggregation of Escherichia coli transconjugants Rubén Monárrez1 and Iruka N. Okeke1,2*
Abstract Objective: Plasmids are key to antimicrobial resistance transmission among enteric bacteria. It is becoming increasingly clear that resistance genes alone do not account for the selective advantage of plasmids and bacterial strains that harbor them. Deletion of a 32 Kb fitness-conferring region of pMB2, a conjugative resistance plasmid, produced a hyper-autoaggregation phenotype in laboratory Escherichia coli. This study sought to determine the genetic basis for hyper-autoaggregation conferred by the pMB2-derived mini-plasmid. Results: The 32 Kb fragment deleted from pMB2 included previously characterized nutrient acquisition genes as well as putative transposase and integrase genes, a 272 bp papB/ pefB-like gene, and several open-reading frames of unknown function. We cloned the papB/ pefB paralogue and found it sufficient to temper the hyper-autoaggregation phenotype. Hyper-autoaggregation conferred by the mini-plasmid did not occur in a fim-negative background. This study has identified and characterized a gene capable of down-regulating host adhesins and has shown that transacting papB/pefB paralogues can occur outside the context of an adhesin cluster. This plasmid-mediated modification of a bacterial host’s colonization program may optimize horizontal transfer of the mobile element bearing the genes. Keywords: Plasmid, PapB, PefB, Fimbrial regulation, Autoaggregation Introduction Bacterial autoaggregation is an adherence phenotype that can manifest in macroscopical clumping. Autoaggregation enhances colonization of some niches but because it is not always advantageous, it is typically regulated transcriptionally or post-transcriptionally by antiaggregation proteins or steric hindrance [1–5]. The Escherichia coli pangenome contains hundreds of known autoaggregation/antiaggregation factors, many of which also function in adherence to other cells and surfaces and have been studied in the context of specific virulent E. coli strains or pathotypes [4]. *Correspondence: [email protected] 2 Department of Pharmaceutical Microbiology, Faculty of Pharmacy, University of Ibadan, Ibadan, Oyo State, Nigeria Full list of author information is available at the end of the article
We recently isolated and sequenced a large multi-drug resistance plasmid from a commensal Escherichia strain in Nigeria and mapped a 32 Kb segment that ameliorated the 125 Kb plasmid’s carrying cost [6]. Here we report that deletion of this portion of plasmid pMB2 produces the smaller pRMKO plasmid that is sufficient to enhance autoaggregation in laboratory E. coli strains in a manner that pMB2 does not. We further demonstrate that the responsible locus was an orphan papB/pefB paralogue, without a cognate fimbrial cluster, and propose that this gene may optimize colonization and transmission in conjugation recipients. The canonical, pathogenicity-island
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