scholarly journals Selective overexpression of the QUTE gene encoding catabolic 3-dehydroquinase in multicopy transformants of Aspergillus nidulans

1990 ◽  
Vol 265 (2) ◽  
pp. 337-342 ◽  
Author(s):  
R K Beri ◽  
S Grant ◽  
C F Roberts ◽  
M Smith ◽  
A R Hawkins
Keyword(s):  
Chlorogenic Acid ◽  
Aspergillus Nidulans ◽  
Gene Cluster ◽  
Quinic Acid ◽  
The Other ◽  
Gene Encoding ◽  
Repressor Gene ◽  
Catabolic Enzymes ◽  
Multiple Copies

The three enzymes necessary to catabolize quinate to protocatechuate are inducible by quinic acid, and transcription of their corresponding genes is controlled by the action of a positively acting activator gene and a negatively acting repressor gene. Transformed strains of Aspergillus nidulans containing multiple copies of the activator gene (QUTA) but single copies of the other QUT genes retain normal regulation of the gene cluster and do not show any overexpression of the three quinic acid catabolic enzymes. Transformed strains containing equal multiple copies of the activator gene (QUTA) and QUTE (encoding catabolic 3-dehydroquinase), but single copies of the other QUT genes, retain normal regulation of the QUT gene cluster, but selectively overexpress the QUTE gene upon quinic acid induction. Data are presented that strongly suggested that the gene QUTG, which is physically located within the QUT gene cluster and for which no function has been identified, is not required for expression of the gene cluster and does not encode a chlorogenic acid esterase.

scholarly journals A Novel Glucosyltransferase Involved in O-Antigen Modification of Shigella flexneri Serotype 1c

2009 ◽  
Vol 191 (21) ◽  
pp. 6612-6617 ◽  
Author(s):  
Robert M. Stagg ◽  
Swee-Seong Tang ◽  
Nils I. A. Carlin ◽  
Kaisar A. Talukder ◽  
Phung D. Cam ◽  
...  
Keyword(s):  
Gene Cluster ◽  
Shigella Flexneri ◽  
Functional Expression ◽  
Transposon Mutagenesis ◽  
The Other ◽  
Bacterial Chromosome ◽  
Gene Encoding ◽  
O Antigen ◽  
Species Analysis

ABSTRACT The O antigen of serotype 1c differs from the unmodified O antigen of serotype Y by the addition of a disaccharide (two glucosyl groups) to the tetrasaccharide repeating unit. It was shown here that addition of the first glucosyl group is mediated by the previously characterized gtrI cluster, which is found within a cryptic prophage at the proA locus in the bacterial chromosome. Transposon mutagenesis was performed to disrupt the gene responsible for addition of the second glucosyl group, causing reversion to serotype 1a. Colony immunoblotting was used to identify the desired revertants, and subsequent sequencing, cloning, and functional expression successfully identified the gene encoding serotype 1c-specific O-antigen modification. This gene (designated gtrIC) was present as part of a three-gene cluster, similar to other S. flexneri glucosyltransferase genes. Relative to the other S. flexneri gtr clusters, the gtrIC cluster is more distantly related and appears to have arrived in S. flexneri from outside the species. Analysis of surrounding sequence suggests that the gtrIC cluster arrived via a novel bacteriophage that was subsequently rendered nonfunctional by a series of insertion events.

Autogenous regulation of the positive regulatory qa-1F gene in Neurospora crassa

1985 ◽  
Vol 5 (12) ◽  
pp. 3593-3599
Author(s):  
V B Patel ◽  
N H Giles
Keyword(s):  
Neurospora Crassa ◽  
Gene Cluster ◽  
Dna Sequences ◽  
Regulatory Gene ◽  
Quinic Acid ◽  
The Other ◽  
Wild Type ◽  
Low Level ◽  
Activator Protein ◽  
Autogenous Regulation

In Neurospora crassa, the qa-1F regulatory gene positively controls transcription of all genes in the quinic acid (qa) gene cluster. qa-1F is transcribed at a low, uninduced level but is subject to strong (50-fold), autogenous regulation as well as to control by the negative regulatory gene, qa-1S, and the inducer quinic acid. Cloned qa-1F DNA sequences hybridize to two related mRNAs of 2.9 and 3.0 kilobases. When wild-type (qa-1F+) cultures are transferred to inducing conditions, qa-1F mRNA increases for 4 h, remains somewhat level, and decreases after 8 to 10 h. That this control is autogenous, i.e., that the qa-1F gene controls the synthesis of its own mRNA, is indicated by the presence of approximately the same low level of qa-1F mRNA in poly(A)+ RNA from noninducible qa-1F- mutant cultures under inducing conditions as that observed in uninduced wild-type cultures. The qa-1S gene also regulates the transcription of qa-1F, since a qa-1S- mutant, whether in noninducing or inducing conditions, contains a level of qa-1F mRNA that corresponds to the low level observed in uninduced wild-type cultures. These results corroborate the hypothesis (M. E. Case and N. H. Giles, Proc. Natl. Acad. Sci. USA 72:553-557, 1975; V. B. Patel, M. Schweizer, C. C. Dykstra, S. R. Kushner, and N. H. Giles, Proc. Natl. Acad. Sci. USA 78:5783-5787, 1981; L. Huiet, Proc. Natl. Acad. Sci. USA 81:1174-1178, 1984) that the qa-1F gene encodes an activator protein and acts positively in controlling transcription of itself and the other qa genes.

scholarly journals Autogenous regulation of the positive regulatory qa-1F gene in Neurospora crassa.

1985 ◽  
Vol 5 (12) ◽  
pp. 3593-3599 ◽  
Author(s):  
V B Patel ◽  
N H Giles
Keyword(s):  
Neurospora Crassa ◽  
Gene Cluster ◽  
Dna Sequences ◽  
Regulatory Gene ◽  
Quinic Acid ◽  
The Other ◽  
Wild Type ◽  
Low Level ◽  
Activator Protein ◽  
Autogenous Regulation

In Neurospora crassa, the qa-1F regulatory gene positively controls transcription of all genes in the quinic acid (qa) gene cluster. qa-1F is transcribed at a low, uninduced level but is subject to strong (50-fold), autogenous regulation as well as to control by the negative regulatory gene, qa-1S, and the inducer quinic acid. Cloned qa-1F DNA sequences hybridize to two related mRNAs of 2.9 and 3.0 kilobases. When wild-type (qa-1F+) cultures are transferred to inducing conditions, qa-1F mRNA increases for 4 h, remains somewhat level, and decreases after 8 to 10 h. That this control is autogenous, i.e., that the qa-1F gene controls the synthesis of its own mRNA, is indicated by the presence of approximately the same low level of qa-1F mRNA in poly(A)+ RNA from noninducible qa-1F- mutant cultures under inducing conditions as that observed in uninduced wild-type cultures. The qa-1S gene also regulates the transcription of qa-1F, since a qa-1S- mutant, whether in noninducing or inducing conditions, contains a level of qa-1F mRNA that corresponds to the low level observed in uninduced wild-type cultures. These results corroborate the hypothesis (M. E. Case and N. H. Giles, Proc. Natl. Acad. Sci. USA 72:553-557, 1975; V. B. Patel, M. Schweizer, C. C. Dykstra, S. R. Kushner, and N. H. Giles, Proc. Natl. Acad. Sci. USA 78:5783-5787, 1981; L. Huiet, Proc. Natl. Acad. Sci. USA 81:1174-1178, 1984) that the qa-1F gene encodes an activator protein and acts positively in controlling transcription of itself and the other qa genes.

Molecular organisation of the quinic acid utilization (QUT) gene cluster in Aspergillus nidulans

1988 ◽  
Vol 214 (2) ◽  
pp. 224-231 ◽  
Author(s):  
Alastair R. Hawkins ◽  
Heather K. Lamb ◽  
Melanie Smith ◽  
John W. Keyte ◽  
Clive F. Roberts
Keyword(s):  
Aspergillus Nidulans ◽  
Gene Cluster ◽  
Quinic Acid ◽  
Molecular Organisation

scholarly journals Front cover: In Vitro Gut Metabolism of [U-13 C]-Quinic Acid, The Other Hydrolysis Product of Chlorogenic Acid

2018 ◽  
Vol 62 (22) ◽  
pp. 1870094
Author(s):  
Martine Naranjo Pinta ◽  
Ivan Montoliu ◽  
Anna-Marja Aura ◽  
Tuulikki Seppänen-Laakso ◽  
Denis Barron ◽  
...  
Keyword(s):  
Chlorogenic Acid ◽  
Hydrolysis Product ◽  
Quinic Acid ◽  
The Other ◽  
Front Cover ◽  
Gut Metabolism

scholarly journals Genetic Regulation of the Quinic Acid Utilization (QUT) Gene Cluster in Aspergillus nidulans

Microbiology ◽  
1988 ◽  
Vol 134 (2) ◽  
pp. 347-358 ◽  
Author(s):  
S. GRANT ◽  
C. F. ROBERTS ◽  
H. LAMB ◽  
M. STOUT ◽  
A. R. HAWKINS
Keyword(s):  
Aspergillus Nidulans ◽  
Gene Cluster ◽  
Genetic Regulation ◽  
Quinic Acid

Aspergillus nidulans Mutants Defective in stc Gene Cluster Regulation

Genetics ◽  
1999 ◽  
Vol 153 (2) ◽  
pp. 715-720 ◽  
Author(s):  
Robert A E Butchko ◽  
Thomas H Adams ◽  
Nancy P Keller
Keyword(s):  
Aspergillus Nidulans ◽  
Gene Cluster ◽  
Growth And Development ◽  
Biosynthetic Pathway ◽  
The Other ◽  
Wild Type ◽  
Norsolorinic Acid ◽  
Genetic Block ◽  
Colored Compound ◽  
Cluster Activity

Abstract The genes involved in the biosynthesis of sterigmatocystin (ST), a toxic secondary metabolite produced by Aspergillus nidulans and an aflatoxin (AF) precursor in other Aspergillus spp., are clustered on chromosome IV of A. nidulans. The sterigmatocystin gene cluster (stc gene cluster) is regulated by the pathway-specific transcription factor aflR. The function of aflR appears to be conserved between ST- and AF-producing aspergilli, as are most of the other genes in the cluster. We describe a novel screen for detecting mutants defective in stc gene cluster activity by use of a genetic block early in the ST biosynthetic pathway that results in the accumulation of the first stable intermediate, norsolorinic acid (NOR), an orange-colored compound visible with the unaided eye. We have mutagenized this NOR-accumulating strain and have isolated 176 Nor- mutants, 83 of which appear to be wild type in growth and development. Sixty of these 83 mutations are linked to the stc gene cluster and are likely defects in aflR or known stc biosynthetic genes. Of the 23 mutations not linked to the stc gene cluster, 3 prevent accumulation of NOR due to the loss of aflR expression.

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