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Wiley InterScience | ||
![]() FEMS Microbiology LettersVolume 148 Issue 1, Pages 107 - 114 Published Online: 17 Jan 2006 © 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved Published on behalf of the Federation of European Microbiological Societies
Abstract | References | Full Text: HTML, PDF (Size: 913K) | Related Articles | Citation Tracking Genetic disruption of the respiratory NADH-ubiquinone reductase of Rhodobacter capsulatus leads to an unexpected photosynthesis-negative phenotype Copyright 1997 Federation of European Microbiological Societies KEYWORDS NADH-ubiquinone oxidoreductase • Lactate dehydrogenase • Photosynthesis deficiency • Respiratory chain •
Rhodobacter capsulatus
ABSTRACTThe NADH-ubiquinone reductase (type I NDH) of Rhodobacter capsulatus is a good model for the genetic study of bacterial homologues of the mitochondrially encoded ND subunits of the mitochondrial complex I. We disrupted the genes nuoH and nuoL which code for the bacterial homologues of subunits ND1 and ND5, respectively, of the mitochondrial enzyme. The corresponding NHK1 and NLK1 mutants present very low membrane-bound NADH-ubiquinone reductase activity. However, these mutants had an unexpected phenotype: while they displayed a nearly normal respiratory growth phenotype on lactate, they were unable to grow photosynthetically under anaerobiosis. Based on the observation of NADH-independent l(−) lactate dehydrogenase (iLDH) activity in membranes of R. capsulatus, we propose a metabolic explanation for this apparently aberrant phenotype. Received 6 December 1996, Revised 13 January 1997, Accepted 13 January 1997 |