Redox regulation of enteric nif expression is independent of the fnr gene product

Hill, Susan

doi:10.1016/0378-1097(85)90261-7

Cited by 8 publications

(8 citation statements)

References 15 publications

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“…Therefore, in addition to the rhizobial homologous Fnr proteins, FnrN and FixK, which are known to be involved in regulation of nitrogen fixation in the symbiotic bacteria (8; see reference 4 and references cited therein), in K. pneumoniae, the transcriptional activator Fnr is apparently also involved in regulation of nitrogen fixation. These results are in contrast to the report of Hill (12), that redox regulation of nif expression in a heterologous E. coli strain is independent of the E. coli fnr gene product. This discrepancy may be due to experimental differences.…”

Section: Discussioncontrasting

confidence: 99%

Fnr Is Required for NifL-Dependent Oxygen Control of nif Gene Expression in Klebsiella pneumoniae

2001

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In Klebsiella pneumoniae, NifA-dependent transcription of nitrogen fixation (nif) genes is inhibited by NifL in response to molecular oxygen and combined nitrogen. We recently showed that K. pneumoniae NifL is a flavoprotein, which apparently senses oxygen through a redox-sensitive, conformational change. We have now studied the oxygen regulation of NifL activity in Escherichia coli and K. pneumoniae strains by monitoring its inhibition of NifA-mediated expression of K. pneumoniae ø(nifH-lacZ) fusions in different genetic backgrounds. Strains of both organisms carrying fnr null mutations failed to release NifL inhibition of NifA transcriptional activity under oxygen limitation: nif induction was similar to the induction under aerobic conditions. When the transcriptional regulator Fnr was synthesized from a plasmid, it was able to complement, i.e., to relieve NifL inhibition in the fnr mutant backgrounds. Hence, Fnr appears to be involved, directly or indirectly, in NifL-dependent oxygen regulation of nif gene expression in K. pneumoniae. The data indicate that in the absence of Fnr, NifL apparently does not receive the signal for anaerobiosis. We therefore hypothesize that in the absence of oxygen, Fnr, as the primary oxygen sensor, activates transcription of a gene or genes whose product or products function to relieve NifL inhibition by reducing the flavin adenine dinucleotide cofactor under oxygen-limiting conditions.

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Section: Discussioncontrasting

confidence: 99%

Fnr Is Required for NifL-Dependent Oxygen Control of nif Gene Expression in Klebsiella pneumoniae

2001

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“…Thus, FNR (the fnr gene product) is the global regulator for anaerobic induction of respiratory enzyme synthesis. Since fnr mutants retain the capacity for anaerobic growth on fermentable carbon sources (Table 4), additional systems are involved in regulation of other anaerobic functions (7,160,178).…”

Section: Physiologymentioning

confidence: 99%

Nitrate respiration in relation to facultative metabolism in enterobacteria.

Stewart¹

1988

Microbiological Reviews

249

162

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“…However, subsequent genetic evidence has shown that the nirA and fnr mutants have closely-linked non-complementing mutations [17]. Some of the problems associated with the nirA mutants may have been due to the presence of multiple mutations affecting anaerobic metabolism [18], and this could also explain the report that one nirA mutant is not complemented by an fnr + plasrnid [19]. Lesions in a gene designated nirR, having the same map position as fnr, and affecting the biosynthesis of nitrite reductase, nitrate reductase, cytochrome css 2, fumarate reductase, hydrogenase and formate hydrogenlyase, have also been described [20,21].…”

Section: Introductionmentioning

confidence: 99%

FNR and its role in oxygen-regulated gene expression in Escherichia coli

Spiro

1990

FEMS Microbiology Letters

205

306

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Bacteria which can grow in different environments have developed regulatory systems which allow them to exploit specific habitats to their best advantage. In the facultative anaerobe Escherichia coli two transcriptional regulators controlling independent networks of oxygen‐regulated gene expression have been identified. One is a two‐component sensor‐regulator system (ArcB‐A), which represses a wide variety of aerobic enzymes under anaerobic conditions. The other is FNR, the transcriptional regulator which is essential for expressing anaerobic respiratory processes. The purpose of this review is to summarize what is known about FNR. The fnr gene was initially defined by the isolation of some pleiotropic mutants which characteristically lacked the ability to use fumarate and nitrate as reducible substrates for supporting anaerobic growth and several other anaerobic respiratory functions. Its role as a transcripitonal regulator emerged from genetic and molecular studies in which its homology with CRP (the cyclic AMP receptor protein which mediates catabolite repression) was established and has since been particularly important in identifying the structural basis of its regulatory specificities. FNR is a member of a growing family of CRP‐related regulatory proteins which have a DNA‐binding domain based on the helix‐turn‐helix structural motif, and a characteristic β‐roll that is involved in nucleotide‐binding in CRP. The FNR protein has been isolated in a monomeric form (Mr 30 000) which exhibits a high but as yet non‐specific affinity for DNA. Nevertheless, the DNA‐recognition site and important residues conferring the functional specificity of FNR have been defined by site‐directed mutagenesis. A consensus for the sequences that are recognized by FNR in the promoter regions of FNR‐regulated genes, has likewise been identified. The basic features of genes and operons regulated by FNR are reviewed, and examples in which FNR functions negatively as an anaerobic repressor as well as positively as an anaerobic activator, are included. Less is known about the way in which FNR senses anoxia and is thereby transformed into its ‘active’s form, but it seems likely that It is clear that oxygen functions as a regulatory signal controlling several important aspects of mitcrobial physiology, and further studies should reveal the molecular basis of the mechanism by which changes in oxygen tension are sensed. The recent identification of FNR homologues in diverse microorganisms points to the widespread importance of this family of regulatory proteins. Moreover, the function of these proteins is not limited to the regulation of anaerobic respiration but includes roles in the regulation of nitrogen fixation and haemolysin biosynthesis. The ability to over‐ride these regulatory mechanisms may have useful biotechnological applications, and it could also be important in controlling pathogenesis. It is anticipated that further studies will provide insights into the way in which these regulatory proteins with common evolut...

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Redox regulation of enteric nif expression is independent of the fnr gene product

Abstract: The fnr gene product, needed for expression of anaerobic catabolism, is not needed for expression of nif in Escherichia coli.

Cited by 8 publications

References 15 publications

Fnr Is Required for NifL-Dependent Oxygen Control of nif Gene Expression in Klebsiella pneumoniae

Fnr Is Required for NifL-Dependent Oxygen Control of nif Gene Expression in Klebsiella pneumoniae

Nitrate respiration in relation to facultative metabolism in enterobacteria.

FNR and its role in oxygen-regulated gene expression in Escherichia coli

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