Contribution of gene loss to the pathogenic evolution of Burkholderia pseudomallei and Burkholderia mallei

Richard A. Moore, Shauna Reckseidler-Zenteno, Heenam Kim, William Nierman, Yan Yu, Apichai Tuanyok, Jonathan Warawa, David DeShazer, Donald E. Woods

Research output: Contribution to journalArticle

90 Citations (Scopus)

Abstract

Burkholderia pseudomallei is the causative agent of melioidosis. Burkholderia thailandensis is a closely related species that can readily utilize L-arabinose as a sole carbon source, whereas B. pseudomallei cannot. We used Tn5-OT182 mutagenesis to isolate an arabinose-negative mutant of B. thailandensis. Sequence analysis of regions flanking the transposon insertion revealed the presence of an arabinose assimilation operon consisting of nine genes. Analysis of the B. pseudomallei chromosome showed a deletion of the operon from this organism. This deletion was detected in all B. pseudomallei and Burkholderia mallei strains investigated. We cloned the B. thailandensis E264 arabinose assimilation operon and introduced the entire operon into the chromosome of B. pseudomallei 406e via homologous recombination. The resultant strain, B. pseudomallei SZ5028, was able to utilize L-arabinose as a sole carbon source. Strain SZ5028 had a significantly higher 50% lethal dose for Syrian hamsters compared to the parent strain 406e. Microarray analysis revealed that a number of genes in a type III secretion system were down-regulated in strain SZ5028 when cells were grown in L-arabinose, suggesting a regulatory role for L-arabinose or a metabolite of L-arabinose. These results suggest that the ability to metabolize L-arabinose reduces the virulence of B. pseudomallei and that the genes encoding arabinose assimilation may be considered antivirulence genes. The increase in virulence associated with the loss of these genes may have provided a selective advantage for B. pseudomallei as these organisms adapted to survival in animal hosts.

Original languageEnglish
Pages (from-to)4172-4187
Number of pages16
JournalInfection and Immunity
Volume72
Issue number7
DOIs
Publication statusPublished - 2004 Jul 1
Externally publishedYes

Fingerprint

Burkholderia mallei
Burkholderia pseudomallei
Arabinose
Genes
Operon
Virulence
Carbon
Chromosomes, Human, 4-5
Melioidosis
Burkholderia
Homologous Recombination
Lethal Dose 50
Mesocricetus
Microarray Analysis
Mutagenesis
Sequence Analysis

ASJC Scopus subject areas

  • Immunology

Cite this

Contribution of gene loss to the pathogenic evolution of Burkholderia pseudomallei and Burkholderia mallei. / Moore, Richard A.; Reckseidler-Zenteno, Shauna; Kim, Heenam; Nierman, William; Yu, Yan; Tuanyok, Apichai; Warawa, Jonathan; DeShazer, David; Woods, Donald E.

In: Infection and Immunity, Vol. 72, No. 7, 01.07.2004, p. 4172-4187.

Research output: Contribution to journalArticle

Moore, RA, Reckseidler-Zenteno, S, Kim, H, Nierman, W, Yu, Y, Tuanyok, A, Warawa, J, DeShazer, D & Woods, DE 2004, 'Contribution of gene loss to the pathogenic evolution of Burkholderia pseudomallei and Burkholderia mallei', Infection and Immunity, vol. 72, no. 7, pp. 4172-4187. https://doi.org/10.1128/IAI.72.7.4172-4187.2004
Moore, Richard A. ; Reckseidler-Zenteno, Shauna ; Kim, Heenam ; Nierman, William ; Yu, Yan ; Tuanyok, Apichai ; Warawa, Jonathan ; DeShazer, David ; Woods, Donald E. / Contribution of gene loss to the pathogenic evolution of Burkholderia pseudomallei and Burkholderia mallei. In: Infection and Immunity. 2004 ; Vol. 72, No. 7. pp. 4172-4187.
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