Previous Article | Next Article ![]()
Journal of Bacteriology, March 2001, p. 1780-1783, Vol. 183, No. 5
Departamento de Bioquímica y
Biología Molecular, Universidad de Córdoba, 14071 Córdoba, Spain,1 and Lehrstuhl
für Biologie der Mikroorganismen, Fakultät für
Biologie, Universität Bochum, D-44780 Bochum,
Germany2
Received 28 July 2000/Accepted 2 December 2000
The phototrophic bacterium Rhodobacter capsulatus is
able to reduce 2,4-dinitrophenol (DNP) to 2-amino-4-nitrophenol
enzymatically and thus can grow in the presence of this uncoupler. DNP
reduction was switched off by glutamine or ammonium, but this
short-term regulation did not take place in a draTG
deletion mutant. Nevertheless, the target of DraTG does not seem to be
the nitrophenol reductase itself since the ammonium shock did not
inactivate the enzyme. In addition to this short-term regulation,
ammonium or glutamine repressed the DNP reduction system. Mutants of
R. capsulatus affected in ntrC or
rpoN exhibited a 10-fold decrease in nitroreductase activity in vitro but almost no DNP activity in vivo. In addition, mutants affected in rnfA or rnfC, which are
also under NtrC control and encode components involved in electron
transfer to nitrogenase, were unable to metabolize DNP. These results
indicate that NtrC regulates dinitrophenol reduction in R. capsulatus, either directly or indirectly, by controlling
expression of the Rnf proteins. Therefore, the Rnf complex seems to
supply electrons for both nitrogen fixation and DNP reduction.
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.5.1780-1783.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Role for draTG and rnf Genes in Reduction
of 2,4-Dinitrophenol by Rhodobacter capsulatus
*
Corresponding author. Mailing address: Departamento de
Bioquímica y Biología Molecular, Edificio C6,
1a Planta, Campus de Rabanales, Universidad de
Córdoba, 14071 Córdoba, Spain. Phone: 34 957218318. Fax: 34 957218592. E-mail: bb1blplr{at}uco.es.
This article has been cited by other articles:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»