Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
Compound
Query: EC:1.6.99.3 (
diaphorase
)
5,903
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We describe the characterization of a mutation of the locus
GLR1
. This mutation allowed for (i) the glucose repression-insensitive synthesis ot the enzymes maltase, galactokinase, alpha-galactosidase, reduced nicotinamide adenine dinucleotide-
cytochrome c reductase
, and cytochrome c oxidase and (ii) growth on maltose in the presence of the gratuitous glucose repressor D-glucosamine. The glucosamine resistance cosegregated with the glucose-insensitive synthesis of the enzymes listed above. In addition, crosses between the glucosamine-resistant mutant and isogenic sensitive strains gave only tetrads containing two resistant and two sensitive spores. Thus, a single pleiotropic mutation is responsible for both phenotypes. We call the locus
GLR1
, for glucose regulation, and the glucose repression-insensitive mutation glr1-1.
...
PMID:Pleiotropic glucose repression-resistant mutation in Saccharomyces carlesbergensis. 720 32
Furfural is a major toxic byproduct found in the hydrolysate of lignocellulosic biomass, which adversely interferes with the growth and ethanol fermentation of
Saccharomyces cerevisiae
. The current study was focused on the impact of cofactor availability derived intracellular redox perturbation on furfural tolerance. Here, three strategies were employed in cofactor conversion in
S. cerevisiae
: (1) heterologous expression of
NADH dehydrogenase
(
NDH
) from
E. coli
which catalyzed the NADH to NAD
+
and increased the cellular sensitivity to furfural, (2) overexpression of
GLR1
, OYE2, ZWF1
, and
IDP1
genes responsible for the interconversion of NADPH and NADP
+
, which enhanced the furfural tolerance, (3) expression of NAD(P)
+
transhydrogenase (
PNTB
) and NAD
+
kinase (
POS5
) which showed a little impact on furfural tolerance. Besides, a substantial redistribution of metabolic fluxes was also observed with the expression of cofactor-related genes. These results indicated that NADPH-based intracellular redox perturbation plays a key role in furfural tolerance, which suggested single-gene manipulation as an effective strategy for enhancing tolerance and subsequently achieving higher ethanol titer using lignocellulosic hydrolysate.
...
PMID:Intracellular Redox Perturbation in
Saccharomyces cerevisiae
Improved Furfural Tolerance and Enhanced Cellulosic Bioethanol Production. 3265 98
