Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A worldwide sample of 37 X chromosomes of Drosophila melanogaster was analyzed with four restriction endonucleases for a 60-kb region of the Notch locus. Any two randomly chosen homologous chromosomes were heterozygous at one in 143 nucleotides (theta = 0.007). The chromosomes that were sampled contained no more than one insertion/deletion. The four insertions and one deletion observed in the 37 chromosomes sampled were located 3' to the Notch transcript; one insertion was represented twice in the sample. The amount of linkage disequilibrium in the Notch region appears to be lower than that of the alcohol dehydrogenase locus in D. melanogaster. The few instances of linkage disequilibrium observed could be due to geographic differentiation of African populations. The genetic variation estimates in the Notch region were comparable with those of the alcohol dehydrogenase region in D. melanogaster, suggesting that molecular genetic variation on the X chromosome is not dramatically reduced by selection against slightly deleterious alleles.
Mol Biol Evol 1988 Jan
PMID:Restriction-map variation in the Notch region of Drosophila melanogaster. 283 76

The alcR positive control gene is necessary for the expression of both alcA (coding for alcohol dehydrogenase ADH I), and aldA (coding for aldehyde dehydrogenase, AldDH) in Aspergillus nidulans. Using a cloned alcR probe and Northern blots analysis we show that: (1) alcR itself is inducible; (2) alcR inducibility depends on the expression of the alcR gene itself; and (3) alcR is subject to carbon catabolite repression and its expression is controlled by the negatively acting creA wide specificity gene. The repression of alcR is sufficient to explain the carbon catabolite repression of ADH I and AldDH.
Mol Microbiol 1987 Nov
PMID:Regulation of alcR, the positive regulatory gene of the ethanol utilization regulon of Aspergillus nidulans. 283 22

The alcohol dehydrogenase (Adh) region from five planitibia subgroup species of Hawaiian picture-wing Drosophila has been cloned. A total of 15 kb of DNA in and around the Adh gene has been compared among the five species. Genetic distances were calculated to determine evolutionary relationships. These distances agree with previous distances determined by protein polymorphism and DNA hybridization techniques and can be interpreted in terms of specific island colonization and speciation (founder) events over the past 5 Myr. Examination of the restriction maps of the cloned Adh region from the five species shows many instances of small deletions, insertion of a transposable element in D. heteroneura, and the existence of a highly variable region on the 3' side of the Adh gene. Clustering relationships and rates of DNA change are calculated and compared with the relationship found for other species of Drosophila.
Mol Biol Evol 1988 Jul
PMID:DNA divergence in and around the alcohol dehydrogenase locus in five closely related species of Hawaiian Drosophila. 284 56

Promoters were isolated at random from the genome of Saccharomyces cerevisiae by using a plasmid that contains a divergently arrayed pair of promoterless reporter genes. A comprehensive library was constructed by inserting random (DNase I-generated) fragments into the intergenic region upstream from the reporter genes. Simple in vivo assays for either reporter gene product (alcohol dehydrogenase or beta-galactosidase) allowed the rapid identification of promoters from among these random fragments. Poly(dA-dT) homopolymer tracts were present in three of five randomly cloned promoters. With two exceptions, each RNA start site detected was 40 to 100 base pairs downstream from a TATA element. All of the randomly cloned promoters were capable of activating reporter gene transcription bidirectionally. Interestingly, one of the promoter fragments originated in a region of the S. cerevisiae rDNA spacer; regulated divergent transcription (presumably by RNA polymerase II) initiated in the same region.
Mol Cell Biol 1988 Oct
PMID:Properties of promoters cloned randomly from the Saccharomyces cerevisiae genome. 284 31

Hepatocytes from 12-day-old rats, pre- and post-natally exposed to alcohol, together with those from pair-fed controls, were isolated and subfractionated in six cell subpopulations on Percoll density gradients. These cells were characterized using a combination of biochemical and stereological methods. The low density cells (F2) mainly showed biochemical and stereological features of perivenous hepatocytes, whereas the heavier cells (F6) were primarily periportal hepatocytes. The alcohol-metabolizing enzymes, alcohol dehydrogenase and aldehyde dehydrogenase (high and low Km) showed more activity in the F2 fraction. Alcohol-altered mitochondria and Golgi apparatus occurred mainly in F2 cells, whereas the endoplasmic reticulum and lysosomes appeared to be more altered in the F6 hepatocytes. Alcohol also induced the appearance of some small hepatocytes, with a well-developed rough endoplasmic reticulum and an increased number of mitochondria. Biochemical data indicated that glutamate dehydrogenase and alanine aminotransferase were more affected in F2 cells from alcohol-treated rats, and that the activity of the ethanol-metabolizing enzymes was alos reduced in these hepatocytes. Our results indicate that alcohol exposure during zonal development in the liver could have a selective effect on specific cell components depending on the acinar zone, and that the perivenous hepatocytes appear to be more damaged under these conditions.
Virchows Arch B Cell Pathol Incl Mol Pathol 1987
PMID:A biochemical and stereological study of neonatal rat hepatocyte subpopulations. Effect of pre- and postnatal exposure to ethanol. 289 91

The Saccharomyces cerevisiae nuclear gene, ADH3, that encodes the mitochondrial alcohol dehydrogenase isozyme ADH III was cloned by virtue of its nucleotide homology to ADH1 and ADH2. Both chromosomal and plasmid-encoded ADH III isozymes were repressed by glucose and migrated heterogeneously on nondenaturing gels. Nucleotide sequence analysis indicated 73 and 74% identity for ADH3 with ADH1 and ADH2, respectively. The amino acid identity between the predicted ADH III polypeptide and ADH I and ADH II was 79 and 80%, respectively. The open reading frame encoding ADH III has a highly basic 27-amino-acid amino-terminal extension relative to ADH I and ADH II. The nucleotide sequence of the presumed leader peptide has a high degree of identity with the untranslated leader regions of ADH1 and ADH2 mRNAs. A strain containing a null allele of ADH3 did not have a detectably altered phenotype. The cloned gene integrated at the ADH3 locus, indicating that this is the structural gene for ADH III.
Mol Cell Biol 1985 Nov
PMID:Isolation and DNA sequence of ADH3, a nuclear gene encoding the mitochondrial isozyme of alcohol dehydrogenase in Saccharomyces cerevisiae. 294 82

An activity gel assay for fructose-1,6-bisphosphatase (FBP), the enzyme catalyzing the final step in gluconeogenesis in yeast, has been developed which can be used in conjunction with spectrophotometric assays to show that it is tightly co-regulated with the inducible alcohol dehydrogenase, ADHII. Both enzymes are repressed coordinately in aerobically grown yeast by the addition of high levels of glucose or ethanol, and induced on minimal medium by the addition of yeast extract. A mutant deficient in FBP segregates independently of the ADHII structural gene locus. This phenomenon is of interest because of the discovery of Ciriacy [(1979) Mol. Gen. Genet. 176, 427-431] of mutants (ccr, or carbon catabolite repression) which repress both FBP and ADHII simultaneously, along with several other enzymes.
 ...
PMID:Alcohol dehydrogenase II and fructose-1,6-bisphosphatase appear to be co-regulated in wild-type yeast. 298 49

Recent sequencing of over 2300 nucleotides containing the alcohol dehydrogenase (Adh) locus in each of 11 Drosophila melanogaster lines makes it possible to estimate the approximate age of the electrophoretic "fast-slow" polymorphism. Our estimates, based on various possible patterns of evolution, range from 610,000 to 3,500,000 years, with 1,000,000 years as a reasonable point estimate. Furthermore, comparison of these sequences with those of the homologous region of D. simulans and D. mauritiana allows us to infer the pattern of evolutionary change of the D. melanogaster sequences. The integrity of the Adh-f electrophoretic alleles as a single lineage is supported by both unweighted pair-group method (UPGMA) and parsimony analyses. However, considerable divergence among the Adh-s lines seems to have preceded the origin of the Adh-f allele. Comparisons of the sequences of D. melanogaster genes with those of D. simulans and D. mauritiana genes suggest that the split between the latter two species occurred more recently than the divergence of some of the present-day Adh-s genes in D. melanogaster. The phylogenetic analyses of the D. melanogaster sequences show that the fast-slow distinction is not perfect, and suggest that intragenic recombination or gene conversion occurred in the evolution of this locus. We extended conventional phylogenetic analyses by using a statistical technique for detecting and characterizing recombination events. We show that the pattern of differentiation of DNA sequences in D. melanogaster is roughly compatible with the neutral theory of molecular evolution.
J Mol Evol 1985
PMID:Phylogenetic analysis of polymorphic DNA sequences at the Adh locus in Drosophila melanogaster and its sibling species. 300 68

A small region of the genome of Drosophila melanogaster has been cloned in a series of overlapping phage. A length of 165 X 10(3) base-pairs of contiguous DNA that spans polytene chromosome region 35A4 to 35B1 and includes the structural gene for alcohol dehydrogenase (Adh) as well as at least two other genes, outspread (osp) and no-ocelli (noc), has been characterized by mapping chromosome aberrations to the DNA. The relationship between osp and Adh is surprising: of nine osp alleles associated with chromosome breakpoints, five map distal (i.e. 5') to Adh and four map proximal (i.e. 3') to this gene. None affects the expression of Adh. As defined by these and other breakpoints, the osp gene spans at least 52 X 10(3) base-pairs and overlaps the Adh gene. The noc gene, as defined by the mapping of nearly 30 breakpoints, is at least 50 X 10(3) base-pairs in size. Alleles of noc and noc- deletions show either of two kinds of interaction with the recessive lethality of l(2)br29ScoR+1, a lethal that maps immediately distal to noc. One class of noc allele is viable when heterozygous with ScoR+1, while the other class is lethal or semi-lethal. Both classes, however, are homozygous or hemizygous viable. The locations of these two classes of noc allele on the DNA fall into two clusters, with those that are viable with ScoR+1 located proximal to those that are not. The physical boundary between these classes lies at a site just distal to that of the breakpoint of the inversion associated with ScoR+1 itself.
J Mol Biol 1985 Dec 20
PMID:Molecular analysis of the Adh region of the genome of Drosophila melanogaster. 300 93

The mutation rate to antimycin A resistance was determined for strains of Sacchromyces cerevisiae lacking a functional copy of the structural gene for alcohol dehydrogenase I (ADH1). One type of mutation that can cause antimycin A resistance in these strains is insertion of the transposable element Ty 5' to ADH2, the structural gene for the glucose-repressed isozyme of alcohol dehydrogenase, resulting in expression of this gene during growth on glucose. Here we show that after growth at 15 or 20 degrees C on glucose, 30% of the antimycin A resistance mutations are Ty insertions at ADH2 and another 65% of the mutations are Ty insertions at ADH4, a new locus identified and cloned as described in this paper. At 30 degrees C only 6% of the mutations are Ty insertions at either of these two loci. In addition, we show that the transposition rate is lower in mating-incompetent (a/alpha) cells than in either haploid or diploid mating-competent cells. Our results suggest that under certain conditions Ty transposition may be a major cause of spontaneous mutations in S. cerevisiae.
Mol Cell Biol 1986 Jan
PMID:Ty insertions at two loci account for most of the spontaneous antimycin A resistance mutations during growth at 15 degrees C of Saccharomyces cerevisiae strains lacking ADH1. 302 38


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>