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J B Gibson

Publications and source records attributed to J B Gibson.

At least 55 records · Page 3Linked to original sources
PubMed1990

Molecular similarity of Drosophila melanogaster alcohol dehydrogenase thermostable alleles from populations on different continents.

Allele specific oligonucleotide probes have been used to show that DNA, amplified by the polymerase chain reaction, from eleven thermostable Adh alleles extracted from populations on different continents contains the triplet TCC, which distinguishes AdhFChD (Fast Chateau Douglas) from AdhF (Fast). The molecular similarity of Adh thermostable alleles suggests that they had a common origin, and it is argued that the mutation probably occurred in China where high frequencies of AdhFChD are found.

Alcohol Dehydrogenase↗
PubMed1990

Aberrant splicing of a naturally occurring alcohol dehydrogenase null activity allele in Drosophila melanogaster.

The DNA sequence of a naturally occurring alcohol dehydrogenase null activity allele, AdhnAC14, has eight extra nucleotides (in two groups of four) in the second intron, commencing six bases 3' from the 5' splice site. A stop codon was also found in exon 2. S1 nuclease protection experiments have shown that the insertions in intron 2 disrupt the correct splicing of intron 2. The null allele produces a transcript approximately 100 bases longer than the normal mature adult transcript, and the amount of the null allele transcript is only about 10% of the normal level.

Alcohol Dehydrogenase↗
PubMed1989

Genetic differentiation in populations of Drosophila melanogaster from the Peoples' Republic of China: comparison with patterns on other continents.

Geographic variation at eight allozyme loci in eight natural populations of Drosophila melanogaster from the People's Republic of China (P.R.C.) was collated with data from Japanese populations and compared with previous reports for other continents. G6pdF, Est-6(1.00) and AdhS were significantly correlated with latitude. Whilst the variation in Est6(1.00) was opposite to that previously reported, AdhS showed latitudinal clines consistent with data from the northern and southern hemispheres. A thermostable variant, AdhFChD, was found at high frequency in the southern P.R.C. populations and it is suggested that the mutation occurred in this region and was then dispersed to other continents.

Acid Phosphatase↗
PubMed1989

Molecular structure of a naturally occurring alcohol dehydrogenase null activity allele in Drosophila melanogaster.

An alcohol dehydrogenase null activity allele, AdhnAH52, extracted from a natural population of Drosophila melanogaster has been cloned and sequenced. Compared with the wild-type consensus sequence, the nucleotide sequence of AdhnAH52 contains eight extra bases in intron 2, adjacent to the 5' splice site. It seems likely that the extra bases result from two structural changes, with a 10-base pair insertion at the same site as a 2-base pair deletion. The insertion includes an 8-base pair duplication of an adjoining region. This structural change alters transcription to give rise to an mRNA which is longer than normal and at 10% of the wild-type level.

Alcohol Dehydrogenase↗
PubMed1988

Synaptonemal complex damage as a measure of genotoxicity at meiosis.

Synaptonemal complex aberrations can provide a sensitive measure of chemical-specific alterations to meiotic chromosomes. Mitomycin C, cyclophosphamide, amsacrine, ellipticine, colchicine, vinblastine sulfate, and cis-platin exposures in mice have been shown to cause various patterns of synaptonemal complex structural damage and synaptic irregularity. These effects are suggestive of abnormal homologue pairing/synapsis/recombination effects which, theoretically, could be implicated in mechanisms leading to aneuploidy and other potentially heritable chromosomal disorders.

Alkaloids↗
PubMed1988

Synaptonemal complex damage induced by clastogenic and anti-mitotic chemicals: implications for non-disjunction and aneuploidy.

Mice were treated with mitomycin C, cyclophosphamide, amsacrine, colchicine, or vinblastine sulfate, and meiotic prophase cells analyzed for synaptonemal complex (SC) damage. All test agents caused synaptonemal complex breakage and synapsis irregularities, although propensities for inducing specific types of damage at S-phase or prophase stages varied among the chemicals. The data indicate that SC analysis can reveal chemical-specific alterations to meiotic homologue pairing/synapsis which have not generally been recognized, and which theoretically may be implicated in non-disjunction.

Aneuploidy↗
PubMed1988

Synaptonemal complex damage in relation to meiotic chromosome aberrations after exposure of male mice to cyclophosphamide.

The genetic implications of induced synaptonemal complex (SC) damage are not known. However, on theoretical grounds, such aberrations could be involved in mechanisms leading to potentially heritable defects. Cyclophosphamide (CP), a chemical reported to cause structural and numerical chromosomal aberrations in the mouse, was used to determine if SC damage observed in meiotic prophase is related to subsequent metaphase chromosomal aberrations. Male mice were injected i.p. with CP. In some instances, mice were also injected simultaneously with tritiated thymidine to label DNA so that cells could be tracked autoradiographically through spermatogenesis. Prophase, primary metaphase (M1), and secondary metaphase (M2) samples were sequentially harvested at appropriate times from the same individual, and nuclei were examined for aberrations. Correlation coefficients between SC and metaphase chromosome aberrations were calculated. The inclusion of tritium labeling increased the number and significance of positive correlations. Positive correlations were found between (1) dose-dependent total SC damage and damage to M1, and to a lesser extent, M2 chromosomes; (2) SC breaks/fragments and M1 chains/rings as well as isochromatid breaks/fragments; (3) SC asynapsis and M1 chromatid breaks/fragments; (4) SC multi-axial configurations and M1 chains/rings as well as isochromatid and chromatid breaks/fragments; and (5) SC multi-axial configurations and M2 hyperploidy. These correlations do not define mechanistic or causal relationships between SC and chromosomal damage. However, taken together with the observation that induced SC damage is many times greater than ensuing metaphase chromosome damage, they substantiate SC analysis as a highly sensitive indicator of potentially heritable effects of this (and presumably other) genotoxic agents.

Aneuploidy↗
PubMed1988

Restriction endonucleases variation in the region of the alcohol dehydrogenase gene: a comparison of null and normal alleles from natural populations of Drosophila melanogaster.

The restriction endonuclease variation in the 12 kb region surrounding twelve Adh null alleles extracted from three Tasmanian populations has been compared with normal alleles from the same populations. Each of the null alleles had the same haplotype as revealed by digestions with eight hexanucleotide restriction enzymes. This haplotype also occurred in 4 of the 46 chromosomes bearing normal alleles which were tested; these four chromosomes with the null allele haplotype carried the AdhS allele. The data suggest that the Adh null alleles from geographically separate populations share a common ancestry and are derived from the same mutation in an AdhS allele.

Alcohol Dehydrogenase↗
PubMed1988

The alcohol dehydrogenase polymorphism of Drosophila melanogaster in relation to environmental ethanol, ethanol tolerance and alcohol dehydrogenase activity.

Ethanol levels in Drosophila breeding sites were higher in a winery storing fortified wines than in nearby grape pressings or in orchard fruits. The relative abundance of D. simulans to D. melanogaster was negatively correlated with ethanol levels. In D. melanogaster there were no significant differences in AdhF frequency between the orchard and winery populations. The ethanol tolerance of wild caught D. melanogaster males paralleled the levels of ethanol in the breeding sites but Adh alleles and ethanol tolerance segregated largely independently of each other. Levels of ADH activity were positively associated with the ethanol tolerance of the different populations and with levels of ethanol in the breeding sites, but it is argued that the ethanol levels are not causative. Flies from inside the winery had higher ADH levels due mainly to greater amounts of ADH-F. The difference in activity persisted for at least one generation in the laboratory. After ten generations of laboratory culture the differences in ethanol tolerance were still present but there were no significant differences in ADH activity.

Alcohol Dehydrogenase↗
PubMed1988

Transcription analysis of alcohol dehydrogenase null alleles from natural populations of Drosophila melanogaster.

Southern analysis of 19 Adh null activity alleles isolated from Tasmanian populations of Drosophila melanogaster have shown that there are no detectable insertions or deletions in an 11.8-kb region that contains the gene. Northern blot analyses of the null alleles have shown that they all produce a transcript about 100 bases longer than that produced by the normal allele and they accumulate a precursor of 1800 bases. The amount of the major transcript produced by the null alleles is about 10% of that produced by normal alleles. The molecular properties of the null alleles suggest that they share a common origin.

Alcohol Dehydrogenase↗
PubMed1987

Synaptonemal complex damage as a measure of chemical mutagen effects on mammalian germ cells.

As heritable chromosome anomalies are implicated in a variety of human disabilities, their induction in germ cells by environmental chemicals is viewed as a threat to health (National Research Council, 1982; Hook, 1983). Synaptonemal complex (SC) analysis is a novel approach for the detection of germ-line chromosomal damage. This sensitive cytological procedure reveals induced structural damage and pairing abnormalities in SCs of meiotic prophase chromosomes, together with other germ-line toxic effects, in the testes of rodents treated with mitomycin C and cyclophosphamide. Our results demonstrate the effectiveness of SC analysis as a rapid and practical in vivo germ-line mutagen assay that lacks many of the short-comings of existing tests.

Animals↗
PubMed1986

The partial characterization of alcohol dehydrogenase null alleles from natural populations of Drosophila melanogaster.

Twenty-three alcohol dehydrogenase (ADH) putative null alleles extracted from four Tasmanian (Australia) populations of Drosophila melanogaster produce no ADH activity and are unable to form active heterodimers with either AdhF or AdhS. Twelve of these nulls were tested by enzyme-linked immunosorbent assay (ELISA) and did not produce any ADH cross-reacting material (CRM). The null homozygotes had similar, but slightly lower, mortalities on ethanol-supplemented media compared to an artificially induced null allele. Heterozygotes between the null alleles and standard AdhF and AdhS alleles had intermediate ADH activity and CRM levels.

Alcohol Dehydrogenase↗