ISSN:
1572-9729
Keywords:
Dichloromethane
;
dichloromethane dehalogenase
;
glutathione S-transferase
;
methylotrophic bacteria
;
Methylobacterium sp.
;
Methylophilus sp.
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Energy, Environment Protection, Nuclear Power Engineering
,
Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
Notes:
Abstract Dichloromethane (DCM) is efficiently utilized as a carbon and energy source by aerobic, Gram-negative, facultative methylotrophic bacteria. It also serves as a sole carbon and energy source for a nitrate-respiringHyphomicrobium sp. and for a strictly anaerobic co-culture of a DCM-fermenting bacterium and an acetogen. The first step of DCM utilization by methylotrophs is catalyzed by DCM dehalogenase which, in a glutathione-dependent substitution reaction, forms inorganic chloride and S-chloromethyl glutathione. This unstable intermediate decomposes to glutathione, inorganic chloride and formaldehyde, a central metabolite of methylotrophic growth. Genetic studies on DCM utilization are beginning to shed some light on questions pertaining to the evolution of DCM dehalogenases and on the regulation of DCM dehalogenase expression. DCM dehalogenase belongs to the glutathione S-transferase supergene family. Analysis of the amino acid sequences of two bacterial DCM dehalogenases reveals 56% identity, and comparison of these sequences to those of glutathione S-transferases indicates a closer relationship to class Theta eukaryotic glutathione S-transferases than to a number of bacterial glutathione S-transferases whose sequences have recently become available.dcmA, the structural gene of the highly substrate-inducible DCM dehalogenase, is carried in most DCM utilizing methylotrophs on large plasmids. InMethylobacterium sp. DM4 its expression is governed bydcmR, a regulatory gene located upstream ofdcmA. dcmR encodes atrans-acting factor which negatively controls DCM dehalogenase formation at the transcriptional level. Our working model thus assumes that thedcmR product is a repressor which, in the absence of DCM, binds to the promoter region ofdcmA and thereby inhibits initiation of transcription.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00696462
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