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Applied and Environmental Microbiology, October 2006, p. 6607-6614, Vol. 72, No. 10
0099-2240/06/$08.00+0     doi:10.1128/AEM.01129-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Coping with Polychlorinated Biphenyl (PCB) Toxicity: Physiological and Genome-Wide Responses of Burkholderia xenovorans LB400 to PCB-Mediated Stress

J. Jacob Parnell,^1,2 Joonhong Park,⁴ Vincent Denef,^1, Tamara Tsoi,¹ Syed Hashsham,^1,3 John Quensen III,^1,2 and James M. Tiedje^1,2*

Center for Microbial Ecology,¹ Department of Crop and Soil Sciences,² Civil and Environmental Engineering, Michigan State University, East Lansing, Michigan 48824,³ Department of Civil and Environmental Engineering, Yonsei University, Seoul 120-749, Republic of Korea⁴

Received 16 May 2006/ Accepted 8 August 2006

The biodegradation of polychlorinated biphenyls (PCBs) relies on the ability of aerobic microorganisms such as Burkholderia xenovorans sp. LB400 to tolerate two potential modes of toxicity presented by PCB degradation: passive toxicity, as hydrophobic PCBs potentially disrupt membrane and protein function, and degradation-dependent toxicity from intermediates of incomplete degradation. We monitored the physiological characteristics and genome-wide expression patterns of LB400 in response to the presence of Aroclor 1242 (500 ppm) under low expression of the structural biphenyl pathway (succinate and benzoate growth) and under induction by biphenyl. We found no inhibition of growth or change in fatty acid profile due to PCBs under nondegrading conditions. Moreover, we observed no differential gene expression due to PCBs themselves. However, PCBs did have a slight effect on the biosurface area of LB400 cells and caused slight membrane separation. Upon activation of the biphenyl pathway, we found growth inhibition from PCBs beginning after exponential-phase growth suggestive of the accumulation of toxic compounds. Genome-wide expression profiling revealed 47 differentially expressed genes (0.56% of all genes) under these conditions. The biphenyl and catechol pathways were induced as expected, but the quinoprotein methanol metabolic pathway and a putative chloroacetaldehyde dehydrogenase were also highly expressed. As the latter protein is essential to conversion of toxic metabolites in dichloroethane degradation, it may play a similar role in the degradation of chlorinated aliphatic compounds resulting from PCB degradation.

Published ahead of print on 21 August 2006.

Present address: Department of Earth and Planetary Sciences, University of California Berkeley, Berkeley, CA.