A putative enoyl-CoA hydratase contributes to biofilm formation and the antibiotic tolerance of Achromobacter xylosoxidans

Lydia C. Cameron; Benjamin Bonis; Chi Q. Phan; Leslie A. Kent; Alysha K. Lee; Ryan C. Hunter

doi:10.1038/s41522-019-0093-6

A putative enoyl-CoA hydratase contributes to biofilm formation and the antibiotic tolerance of Achromobacter xylosoxidans

Lydia C. Cameron
, Benjamin Bonis
, Chi Q. Phan
, Leslie A. Kent
, Alysha K. Lee
, Ryan C. Hunter

Microbiology

Research output: Contribution to journal › Article › peer-review

18 Scopus citations

Abstract

Achromobacter xylosoxidans has attracted increasing attention as an emerging pathogen in patients with cystic fibrosis. Intrinsic resistance to several classes of antimicrobials and the ability to form robust biofilms in vivo contribute to the clinical manifestations of persistent A. xylosoxidans infection. Still, much of A. xylosoxidans biofilm formation remains uncharacterized due to the scarcity of existing genetic tools. Here we demonstrate a promising genetic system for use in A. xylosoxidans; generating a transposon mutant library which was then used to identify genes involved in biofilm development in vitro. We further described the effects of one of the genes found in the mutagenesis screen, encoding a putative enoyl-CoA hydratase, on biofilm structure and tolerance to antimicrobials. Through additional analysis, we find that a fatty acid signaling compound is essential to A. xylosoxidans biofilm ultrastructure and maintenance. This work describes methods for the genetic manipulation of A. xylosoxidans and demonstrated their use to improve our understanding of A. xylosoxidans pathophysiology.

Original language	English (US)
Article number	20
Journal	NPJ biofilms and microbiomes
Volume	5
Issue number	1
DOIs	https://doi.org/10.1038/s41522-019-0093-6
State	Published - Dec 1 2019

Bibliographical note

Funding Information:
pGGA008 (Addgene plasmid #48817) was a gift from Dr. Jan Lohmann (Heidelberg). We thank Clayton Summitt for assistance with data analysis and other members of the Hunter lab for critical review of the manuscript. Parts of this work were carried out in the Characterization Facility, University of Minnesota, which receives partial support from NSF through the Materials Research Science and Engineering Centers (MRSEC) program. This study was supported by the University of Minnesota, a NHLBI Pathway to Independence award to RCH, American Society for Microbiology Undergraduate Research Fellowships to AKL and LAK.

Publisher Copyright:
© 2019, The Author(s).

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title = "A putative enoyl-CoA hydratase contributes to biofilm formation and the antibiotic tolerance of Achromobacter xylosoxidans",

abstract = "Achromobacter xylosoxidans has attracted increasing attention as an emerging pathogen in patients with cystic fibrosis. Intrinsic resistance to several classes of antimicrobials and the ability to form robust biofilms in vivo contribute to the clinical manifestations of persistent A. xylosoxidans infection. Still, much of A. xylosoxidans biofilm formation remains uncharacterized due to the scarcity of existing genetic tools. Here we demonstrate a promising genetic system for use in A. xylosoxidans; generating a transposon mutant library which was then used to identify genes involved in biofilm development in vitro. We further described the effects of one of the genes found in the mutagenesis screen, encoding a putative enoyl-CoA hydratase, on biofilm structure and tolerance to antimicrobials. Through additional analysis, we find that a fatty acid signaling compound is essential to A. xylosoxidans biofilm ultrastructure and maintenance. This work describes methods for the genetic manipulation of A. xylosoxidans and demonstrated their use to improve our understanding of A. xylosoxidans pathophysiology.",

author = "Cameron, \{Lydia C.\} and Benjamin Bonis and Phan, \{Chi Q.\} and Kent, \{Leslie A.\} and Lee, \{Alysha K.\} and Hunter, \{Ryan C.\}",

note = "Funding Information: pGGA008 (Addgene plasmid \#48817) was a gift from Dr. Jan Lohmann (Heidelberg). We thank Clayton Summitt for assistance with data analysis and other members of the Hunter lab for critical review of the manuscript. Parts of this work were carried out in the Characterization Facility, University of Minnesota, which receives partial support from NSF through the Materials Research Science and Engineering Centers (MRSEC) program. This study was supported by the University of Minnesota, a NHLBI Pathway to Independence award to RCH, American Society for Microbiology Undergraduate Research Fellowships to AKL and LAK. Publisher Copyright: {\textcopyright} 2019, The Author(s).",

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AU - Lee, Alysha K.

AU - Hunter, Ryan C.

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N2 - Achromobacter xylosoxidans has attracted increasing attention as an emerging pathogen in patients with cystic fibrosis. Intrinsic resistance to several classes of antimicrobials and the ability to form robust biofilms in vivo contribute to the clinical manifestations of persistent A. xylosoxidans infection. Still, much of A. xylosoxidans biofilm formation remains uncharacterized due to the scarcity of existing genetic tools. Here we demonstrate a promising genetic system for use in A. xylosoxidans; generating a transposon mutant library which was then used to identify genes involved in biofilm development in vitro. We further described the effects of one of the genes found in the mutagenesis screen, encoding a putative enoyl-CoA hydratase, on biofilm structure and tolerance to antimicrobials. Through additional analysis, we find that a fatty acid signaling compound is essential to A. xylosoxidans biofilm ultrastructure and maintenance. This work describes methods for the genetic manipulation of A. xylosoxidans and demonstrated their use to improve our understanding of A. xylosoxidans pathophysiology.

AB - Achromobacter xylosoxidans has attracted increasing attention as an emerging pathogen in patients with cystic fibrosis. Intrinsic resistance to several classes of antimicrobials and the ability to form robust biofilms in vivo contribute to the clinical manifestations of persistent A. xylosoxidans infection. Still, much of A. xylosoxidans biofilm formation remains uncharacterized due to the scarcity of existing genetic tools. Here we demonstrate a promising genetic system for use in A. xylosoxidans; generating a transposon mutant library which was then used to identify genes involved in biofilm development in vitro. We further described the effects of one of the genes found in the mutagenesis screen, encoding a putative enoyl-CoA hydratase, on biofilm structure and tolerance to antimicrobials. Through additional analysis, we find that a fatty acid signaling compound is essential to A. xylosoxidans biofilm ultrastructure and maintenance. This work describes methods for the genetic manipulation of A. xylosoxidans and demonstrated their use to improve our understanding of A. xylosoxidans pathophysiology.

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A putative enoyl-CoA hydratase contributes to biofilm formation and the antibiotic tolerance of Achromobacter xylosoxidans

Abstract

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