Previous Article | Next Article ![]()
Applied and Environmental Microbiology, July 2009, p. 4248-4253, Vol. 75, No. 13
0099-2240/09/$08.00+0 doi:10.1128/AEM.00203-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
,
,
Jong-Chan Chae,2,
,¶
Gerben J. Zylstra,1,2 and
Max M. Häggblom1,2*
Department of Biochemistry and Microbiology,1 Biotechnology Center for Agriculture and the Environment, School of Environmental and Biological Sciences, Rutgers University, New Brunswick, New Jersey 089012
Received 28 January 2009/ Accepted 25 April 2009
A sulfate-reducing phenol-degrading bacterium, strain AK1, was isolated from a 2-bromophenol-utilizing sulfidogenic estuarine sediment enrichment culture. On the basis of phylogenetic analysis of the 16S rRNA gene and DNA homology, strain AK1 is most closely related to Desulfobacterium anilini strain Ani1 (= DSM 4660T). In addition to phenol, this organism degrades a variety of other aromatic compounds, including benzoate, 2-hydroxybenzoate, 4-hydroxybenzoate, 4-hydroxyphenylacetate, 2-aminobenzoate, 2-fluorophenol, and 2-fluorobenzoate, but it does not degrade aniline, 3-hydroxybenzoate, 4-cyanophenol, 2,4-dihydroxybenzoate, monohalogenated phenols, or monohalogenated benzoates. Growth with sulfate as an electron acceptor occurred with acetate and pyruvate but not with citrate, propionate, butyrate, lactate, glucose, or succinate. Strain AK1 is able to use sulfate, sulfite, and thiosulfate as electron acceptors. A putative phenylphosphate synthase gene responsible for anaerobic phenol degradation was identified in strain AK1. In phenol-grown cultures inducible expression of the ppsA gene was verified by reverse transcriptase PCR, and 4-hydroxybenzoate was detected as an intermediate. These results suggest that the pathway for anaerobic degradation of phenol in D. anilini strain AK1 proceeds via phosphorylation of phenol to phenylphosphate, followed by carboxylation to 4-hydroxybenzoate. The details concerning such reaction pathways in sulfidogenic bacteria have not been characterized previously.
Published ahead of print on 1 May 2009.
Supplemental material for this article may be found at http://aem.asm.org/.
Y.-B.A. and J.-C.C. contributed equally to this work.
Present address: Division of Microbiology, National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR 72079-9502.
¶ Present address: Division of Biotechnology, College of Environmental and Bioresource Sciences, Chonbuk National University, Iksan 570-752, South Korea.
Copyright © 2010 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»