Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.7.1.2 (
nitrate reductase
)
3,861
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
This paper reports three lines of evidence to demonstrate the presence of heterotrimeric G-proteins in maize and their involvement in the regulation of
nitrate reductase
gene expression by light: (1) Southern blot analysis of maize genomic DNA using a human Ha-ras cDNA probe revealed specific bands indicating the presence of G-protein (alpha subunit) gene(s) in maize. Northern blot analysis of maize total RNA using the same probe revealed that the putative Galpha gene(s) is transcriptionally active. (2) Western blots containing purified plasma membrane proteins from maize leaves showed specific binding of gamma [35S]-labeled GTP in a red light-dependent manner, indicating the involvement of G-proteins in mediating the light signal. The size of the putative Galpha gene product (approximately 45 kDa) indicates that it may be a heterotrimeric G-protein. (3)
Cholera
toxin mimicked the effect of red light to enhance the transcript levels of
nitrate reductase
(NR), indicating that G-proteins may mediate light regulation of NR gene expression.
...
PMID:Light regulation of nitrate reductase gene expression in maize involves a G-protein. 1054 30
Vibrio cholerae
lives in different habitats, varying from aquatic ecosystems to the human intestinal tract. The organism has acquired a set of electron transport pathways for aerobic and anaerobic respiration that enable adaptation to the various environmental conditions. We have inactivated the V. cholerae ccmE gene, which is required for cytochrome c biogenesis. The resulting strain is deficient of all c-type cytochromes and allows us to characterize the physiological role of these proteins. Under aerobic conditions in rich medium, V. cholerae produces at least six c-type cytochromes, none of which is required for growth. Wild-type V. cholerae produces active fumarate reductase, trimethylamine N-oxide reductase, cbb3 oxidase, and
nitrate reductase
, of which only the fumarate reductase does not require maturation of c-type cytochromes. The reduction of nitrate in the medium resulted in the accumulation of nitrite, which is toxic for the cells. This suggests that V. cholerae is able to scavenge nitrate from the environment only in the presence of other nitrite-reducing organisms. The phenotypes of cytochrome c-deficient V. cholerae were used in a transposon mutagenesis screening to search for additional genes required for cytochrome c maturation. Over 55,000 mutants were analyzed for
nitrate reductase
and cbb3 oxidase activity. No transposon insertions other than those within the ccm genes for cytochrome c maturation and the dsbD gene, which encodes a disulphide bond reductase, were found. In addition, the role of a novel CcdA-like protein in cbb3 oxidase assembly is discussed.
...
PMID:Cytochrome c maturation and the physiological role of c-type cytochromes in Vibrio cholerae. 1610 41
To survive and proliferate in the absence of oxygen, many enteric pathogens can undergo anaerobic respiration within the host by using nitrate (NO
3
-
) as an electron acceptor
1,2
. In these bacteria, NO
3
-
is typically reduced by a
nitrate reductase
to nitrite (NO
2
-
), a toxic intermediate that is further reduced by a nitrite reductase
3
. However,
Vibrio cholerae
, the intestinal pathogen that causes
cholera
, lacks a nitrite reductase, leading to NO
2
-
accumulation during nitrate reduction
4
. Thus, V. cholerae is thought to be unable to undergo NO
3
-
-dependent anaerobic respiration
4
. Here, we show that during hypoxic growth, NO
3
-
reduction in V. cholerae divergently affects bacterial fitness in a manner dependent on environmental pH. Remarkably, in alkaline conditions, V. cholerae can reduce NO
3
-
to support population growth. Conversely, in acidic conditions, accumulation of NO
2
-
from NO
3
-
reduction simultaneously limits population expansion and preserves cell viability by lowering fermentative acid production. Interestingly, other bacterial species such as Salmonella typhimurium, enterohaemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium also reproduced this pH-dependent response, suggesting that this mechanism might be conserved within enteric pathogens. Our findings explain how a bacterial pathogen can use a single redox reaction to divergently regulate population expansion depending on the fluctuating environmental pH.
...
PMID:Anaerobic nitrate reduction divergently governs population expansion of the enteropathogen Vibrio cholerae. 3027 12
