Structural alteration of linear plasmids encoding the genes for polychlorinated biphenyl degradation in Rhodococcus strain RHA1

Polychlorinated biphenyl (PCB) tolerant derivatives of a strong PCB degrader, Rhodococcus strain RHA1, were selected after growth in the presence of 100 micrograms/ml PCBs. Some of the derivatives did not grow on biphenyl but accumulated a yellow coloured metabolite suggesting a defect in the meta-r...

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Bibliographic Details
Published in:Antonie van Leeuwenhoek 1998-10, Vol.74 (1-3), p.169-173
Main Authors: Fukuda, M, Shimizu, S, Okita, N, Seto, M, Masai, E
Format: Article
Language:English
Subjects:
Benzene Derivatives - metabolism
Biphenyl Compounds - metabolism
Brackish
Derivatives
Enzyme Induction
Freshwater
Genes, Bacterial
Hydrolases
Marine
Metabolites
PCB
Plasmids
Polychlorinated biphenyls
Polychlorinated Biphenyls - metabolism
Rhodococcus
Rhodococcus - genetics
Rhodococcus - metabolism
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Summary:Polychlorinated biphenyl (PCB) tolerant derivatives of a strong PCB degrader, Rhodococcus strain RHA1, were selected after growth in the presence of 100 micrograms/ml PCBs. Some of the derivatives did not grow on biphenyl but accumulated a yellow coloured metabolite suggesting a defect in the meta-ring-cleavage compound hydrolase step encoded by the bphD gene. Other derivatives failed to grow on biphenyl and exhibited little PCB transformation activity suggesting a defect in the initial ring-hydroxylation dioxygenase step encoded by the bphA gene. These organisms had a structural alteration in the linear plasmids coding for the bph genes in RHA1, which included the bph gene deletion. When a bphD containing plasmid was introduced into a tolerant derivative, RCD1, which was shown to have bphD deletion, the defect in the growth on biphenyl of RCD1 was overcome. The bph gene deletion seems to play a key role in these tolerant derivatives thereby suggesting that the toxic metabolic intermediate would be a main cause of the growth inhibition of RHA1 in the presence of high concentration PCBs.
ISSN:0003-6072
1572-9699
DOI:10.1023/a:1001732718159