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Infection and Immunity, March 2009, p. 935-942, Vol. 77, No. 3
0019-9567/09/$08.00+0 doi:10.1128/IAI.00929-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
Role of Melanin Pigment in Expression of Vibrio cholerae Virulence Factors
Soni Priya Valeru,1,
Pramod Kumar Rompikuntal,1,
Takahiko Ishikawa,1
Karolis Vaitkevicius,1
Åsa Sjöling,2
Nadia Dolganov,3
Jun Zhu,4
Gary Schoolnik,3 and
Sun Nyunt Wai1*
Department of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden,1 Department of Microbiology and Immunology, Institute of Biomedicine, University of Gothenburg, Box 435, 405 30, Sweden,2 Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California,3 Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 191044
Received 25 July 2008/ Returned for modification 31 August 2008/ Accepted 8 December 2008
We identified the mutated gene locus in a pigment-overproducing Vibrio cholerae mutant of strain A1552. The deduced gene product is suggested to be an oxidoreductase based on partial homology to putative homogentisate 1,2-dioxygenase in Pseudomonas aeruginosa and Mesorhizobium loti, and we propose that the gene VC1345 in the V. cholerae genome be denoted hmgA in accordance with the nomenclature for other species. The hmgA::mini-Tn5 mutant showed a nonpigmented phenotype after complementation with a plasmid clone carrying the WT hmgA+ locus. Microarray transcription analysis revealed that expression of hmgA and the neighboring genes encoding a postulated two-component sensor system was growth phase dependent. Results from quantitative reverse transcription-PCR analysis showed that hmgA operon expression was reduced in the rpoS mutant, but pigment production by the WT V. cholerae or the hmgA mutant was not detectably influenced by the stationary-phase regulator RpoS. The pigmented mutant showed increased UV resistance in comparison with the WT strain. Interestingly, the pigment-producing mutant expressed more toxin-coregulated pilus and cholera toxin than WT V. cholerae. Moreover, the hmgA mutant showed a fivefold increase in the ability to colonize the intestines of infant mice. A possible mechanism by which pigment production might cause induction of the ToxR regulon due to generation of hydrogen peroxide was supported by results from tests showing that externally supplied H2O2 led to higher TcpA levels. Taken together, our findings suggest that melanin pigment formation may play a role in V. cholerae virulence factor expression.
* Corresponding author. Mailing address: Department of Molecular Biology, Umeå University, SE-901 87 Umeå, Sweden. Phone: 46-90-7856704. Fax: 46-90-772630. E-mail: sun.nyunt.wai{at}molbiol.umu.se
Published ahead of print on 22 December 2008.
S.P.V. and P.K.R. contributed equally to the work.
Infection and Immunity, March 2009, p. 935-942, Vol. 77, No. 3
0019-9567/09/$08.00+0 doi:10.1128/IAI.00929-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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