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Journal of Bacteriology, August 2007, p. 5996-6010, Vol. 189, No. 16
0021-9193/07/$08.00+0 doi:10.1128/JB.00368-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.
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Marcin P. Joachimiak,1,2,
Adam P. Arkin,1,2,4
Sharon E. Borglin,1,5
Paramvir S. Dehal,1,2
Romy Chakraborty,1,5
Jil T. Geller,1,5
Terry C. Hazen,1,5
Qiang He,1,6,
Dominique C. Joyner,1,5
Vincent J. J. Martin,1,2,¶
Judy D. Wall,1,7
Zamin Koo Yang,1,6
Jizhong Zhou,1,6,8 and
Jay D. Keasling1,2,3,4*
Virtual Institute of Microbial Stress and Survival,1 Physical Biosciences Division, Lawrence Berkeley National Laboratory, Berkeley, California,2 Department of Chemical Engineering, University of California, Berkeley, California,3 Department of Bioengineering, University of California, Berkeley, California,4 Earth Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California,5 Environmental Sciences Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee,6 Biochemistry and Molecular Microbiology & Immunology Departments, University of Missouri, Columbia, Missouri,7 Institute for Environmental Genomics and Department of Botany and Microbiology, Oklahoma University, Norman, Oklahoma8
Received 12 March 2007/ Accepted 20 May 2007
The responses of the anaerobic, sulfate-reducing organism Desulfovibrio vulgaris Hildenborough to low-oxygen exposure (0.1% O2) were monitored via transcriptomics and proteomics. Exposure to 0.1% O2 caused a decrease in the growth rate without affecting viability. Concerted upregulation of the predicted peroxide stress response regulon (PerR) genes was observed in response to the 0.1% O2 exposure. Several of the candidates also showed increases in protein abundance. Among the remaining small number of transcript changes was the upregulation of the predicted transmembrane tetraheme cytochrome c3 complex. Other known oxidative stress response candidates remained unchanged during the low-O2 exposure. To fully understand the results of the 0.1% O2 exposure, transcriptomics and proteomics data were collected for exposure to air using a similar experimental protocol. In contrast to the 0.1% O2 exposure, air exposure was detrimental to both the growth rate and viability and caused dramatic changes at both the transcriptome and proteome levels. Interestingly, the transcripts of the predicted PerR regulon genes were downregulated during air exposure. Our results highlight the differences in the cell-wide responses to low and high O2 levels in D. vulgaris and suggest that while exposure to air is highly detrimental to D. vulgaris, this bacterium can successfully cope with periodic exposure to low O2 levels in its environment.
Published ahead of print on 1 June 2007.
Supplemental material for this article may be found at http://jb.asm.org/.
A.M.R. and M.P.J. contributed equally to this study.
Present address: Department of Civil and Environmental Engineering, Temple University, Philadelphia, PA 19122.
¶ Present address: Biology Department, Centre for Structural and Functional Genomics, Concordia University, 7141 Sherbrooke West, Montreal, Quebec, Canada H4B 1R6.
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