Molecular analysis of alcohol dehydrogenase electromorphs in wild type and transformed Drosophila melanogaster

1988 ◽  
Vol 150 (2) ◽  
pp. 655-664 ◽  
Author(s):  
Mark A. Batzer ◽  
Trent D. Desselle ◽  
Mark D. Brennan ◽  
William R. Lee ◽  
Bruce Tedeschi
Keyword(s):  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Molecular Analysis ◽  
Wild Type

scholarly journals The molecular analysis of the el-noc complex of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 126 (1) ◽  
pp. 105-119
Author(s):  
T Davis ◽  
J Trenear ◽  
M Ashburner
Keyword(s):  
Drosophila Melanogaster ◽  
Molecular Analysis ◽  
Molecular Level ◽  
Wild Type ◽  
Distinct Phenotype

Abstract The el-noc complex spans a distance of about 200 kb on chromosome 2L. It consists of three discrete genetic regions el, l(2)35Ba and noc, each of which has a distinct phenotype when mutant. The noc locus itself is complex, including three separate regions. The el locus has been characterized by mapping 30 aberration breakpoints to the DNA. It extends over a distance of about 80 kb. It can be divided into two parts by the aberrations In(2LR)DTD128 and T(Y;2)A80. These break between two sets of el alleles yet are both phenotypically wild type for elbow. The simplest explanation is that el consists of two transcription units elA and elB. The locus pu, which appears to be unrelated to the el-noc complex, is found to map between the two el loci very close to elB (the distal el locus). The loci l(2)35Ba and nocA have been separated by only two l(2)35Ba+nocA- deletions and a nocA- inversion. No l(2)35Ba-nocA+ aberrations have been found. At the molecular level these loci are found to occupy almost the same region, and are probably identical.

scholarly journals Identification of cis-regulatory elements required for larval expression of the Drosophila melanogaster alcohol dehydrogenase gene.

Genetics ◽  
1990 ◽  
Vol 124 (3) ◽  
pp. 637-646 ◽  
Author(s):  
V Corbin ◽  
T Maniatis
Keyword(s):  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Dna Sequences ◽  
Regulatory Elements ◽  
Malpighian Tubules ◽  
Proximal Promoter ◽  
Start Site ◽  
Wild Type ◽  
Tissue Specific ◽  
Adh Gene

Abstract The Alcohol dehydrogenase (Adh) genes of two distantly related species, Drosophila melanogaster and Drosophila mulleri, display similar, but not identical, patterns of tissue-specific expression in larvae and adults. The regulatory DNA sequences necessary for wild-type Adh expression in D. mulleri larvae were previously reported. In this paper we present an analysis of the DNA sequences necessary for wild-type Adh expression in D. melanogaster larvae. We show that transcription from the proximal promoter of the melanogaster Adh gene is regulated by a far upstream enhancer and two or more elements near the transcription start site. The enhancer is tissue specific and stimulates transcription to high levels in fat body and to lower levels in midgut and malpighian tubules whether linked to the proximal promoter or to a heterologous promoter. The enhancer activity localized to at least two discrete regions dispersed over more than 1.7 kb of DNA. Deletion of any one of these subregions reduces Adh transcription in all three larval tissues. Similarly, two regions immediately upstream of the proximal promoter start site are necessary for wild-type transcription levels in all three tissues. Thus, each of the identified regulatory elements is sufficient for low levels of Adh gene expression in all three larval tissues, but maximal levels of expression requires the entire set.

scholarly journals Unequal crossing-over within the B duplication of Drosophila melanogaster: a molecular analysis

1991 ◽  
Vol 57 (2) ◽  
pp. 105-111 ◽  
Author(s):  
Stuart I. Tsubota
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Element ◽  
Molecular Analysis ◽  
Recombination Event ◽  
Tandem Duplication ◽  
Molecular Data ◽  
Crossing Over ◽  
Wild Type ◽  
Unequal Crossing Over ◽  
Extreme Form

SummaryThe B mutation is associated with a tandem duplication of 16A1–16A7. It is unstable, mutating to wild type and to a more extreme form at a frequency of one in 1000 to 3000. The reversion to wild type is associated with the loss of one copy of the duplication, whereas the mutation to extreme B is associated with a triplication of the region. The instability of B has been attributed to unequal crossing-over between the two copies of the duplication. Recent molecular data show that there is a transposable element, B104, between the two copies of the duplication and support the hypothesis that this element generated the duplication via a recombination event. These data suggest that unequal crossing-over within the duplication may not be the cause of the instability of B. Instead, the instability may be caused by a recombination event involving the B104 element. This issue was addressed using probes for the DNA on either side of the B104 element at the B breakpoint. All of the data indicate that the B104 element is not involved in the instability of B and support the original unequal crossing-over model.

scholarly journals Insertion of the retroposable element, jockey, near the Adh gene of Drosophila melanogaster is associated with altered gene expression

1996 ◽  
Vol 68 (3) ◽  
pp. 203-209 ◽  
Author(s):  
Lisa D. White ◽  
James W. Jacobson
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Insertion Mutation ◽  
Activity Levels ◽  
Mrna Levels ◽  
Wild Type ◽  
Reporter System ◽  
Wild Type Counterpart ◽  
Altered Gene

SummaryThe alcohol dehydrogenase (Adh) gene of Drosophila melanogaster is well suited to be a gene expression reporter system. Adh produces a measurable phenotype at both the enzyme and mRNA levels. We recovered a spontaneous transposable element (TE) insertion mutation near the Adh gene. The insertion is a truncated retroposable element, jockey, inserted upstream of the adult Adh enhancer region. Comparisons between the Adhjockey allele and its direct wild-type ancestral allele were made in an isogenic background (i.e. identical cis and trans factors). Differences in Adhjockey expression compared with the wild-type can be attributed solely to the presence of the jockey element. This jockey insertion results in a decrease in adult mRNA transcript levels in the Adhjockey homozygous lines relative to the wild-type counterpart and accounts for a correlated decrease in alcohol dehydrogenase (ADH) enzyme activity. The larval ADH activity levels are not detectably different.

Molecular Analysis of the Alleles of Alcohol Dehydrogenase Along a Cline in Drosophila Melanogaster. I. Maine, North Carolina, and Florida

Evolution ◽  
1989 ◽  
Vol 43 (2) ◽  
pp. 393 ◽  
Author(s):  
Gail M. Simmons ◽  
Martin E. Kreitman ◽  
William F. Quattlebaum ◽  
Naohiko Miyashita
Keyword(s):  
North Carolina ◽  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Molecular Analysis

scholarly journals A deleted hobo element is involved in the unstable thermosensitive vgal mutation at the vestigial locus in Drosophila melanogaster

1993 ◽  
Vol 61 (3) ◽  
pp. 171-176 ◽  
Author(s):  
C. Bazin ◽  
J. Williams ◽  
J. Bell ◽  
J. Silber
Keyword(s):  
Drosophila Melanogaster ◽  
Natural Population ◽  
Molecular Analysis ◽  
Terminal Repeat ◽  
Wild Type ◽  
Wild Type Phenotype ◽  
Hobo Element ◽  
Genetic Structures

SummaryWe have described a new unstable mutant of the vestigial locus isolated from a natural population. From this mutant, vestigialalmost (vgal), wild-type (vgal+), and extreme (vgext), alleles arose spontaneously. The molecular analysis of vgal shows that the mutation is due to a 1874 bp hobo element inserted in a vestigial intron. Two distinct kinds of events lead a wild-type phenotype. Three independent vgal+ alleles result from an excision of the hobo element and two other vgal+ alleles have further deletions of hobo sequence. The sequence of one of them shows a 1516 bp hobo insertion at the same place and in the same orientation as the 1874 bp insertion. In the vgext alleles, we found a 5′ or 3′ variably sized deletion of vg sequences. One of them, which has been cloned and sequenced, has a deletion finishing exactly at the left terminal repeat′ hobo element. The genetic implications of these different genetic structures are discussed.

scholarly journals Insertion of a copia element 5' to the Drosophila melanogaster alcohol dehydrogenase gene (adh) is associated with altered developmental and tissue-specific patterns of expression.

Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 787-794
Author(s):  
D J Strand ◽  
J F McDonald
Keyword(s):  
Drosophila Melanogaster ◽  
Alcohol Dehydrogenase ◽  
Transcriptional Start Site ◽  
Adult Life ◽  
Life Stages ◽  
Start Site ◽  
Wild Type ◽  
Dehydrogenase Gene ◽  
In Trans ◽  
Copia Element

Abstract The Drosophila melanogaster alcohol dehydrogenase gene (adh) is under the control of two separate promoters (proximal and distal) which are preferentially utilized at the larval and adult life stages, respectively. A variant alcohol dehydrogenase allele (RI-42) isolated from a natural population contains a copia retroviral-like transposable element inserted 240 bp upstream from the distal (adult) adh transcriptional start site. Levels of adh transcripts in the RI-42 variant are reduced in tissues and at life stages where copia is actively expressed and are affected in trans- by mutant alleles at the suppressor-of-white-apricot (su(wa] and suppressor-of-forked (su(f] loci. These suppressor genes have no effect on adh expression in wild-type Drosophila.

scholarly journals Molecular Analysis of Diepoxybutane-Induced Mutations at the rosy Locus of Drosophila melanogaster

Genetics ◽  
1987 ◽  
Vol 115 (2) ◽  
pp. 323-331
Author(s):  
J T Reardon ◽  
C A Liljestrand-Golden ◽  
R L Dusenbery ◽  
P D Smith
Keyword(s):  
Drosophila Melanogaster ◽  
Molecular Analysis ◽  
Molecular Level ◽  
Genetic Material ◽  
Regulatory Sequences ◽  
Wild Type ◽  
Induced Mutations ◽  
Base Pairs ◽  
Restriction Patterns ◽  
Induced Mutants

ABSTRACT We have analyzed at the molecular level diepoxybutane-induced mutants determined to have lesions affecting expression of the ry locus. Of the 21 mutants analyzed here, genetic analysis suggested that five were putative deficiencies involving ry and adjacent lethal loci. However, molecular analysis confirmed that only two of these five putative deficiencies were in fact deletions detectable by the methods used in the analysis. The remaining 16 mutants were viable as homozygotes, suggesting that their lesions were confined to the ry locus. Seven of these 16 intragenic mutants were determined to be deletions of genetic material as evidenced by altered restriction patterns relative to the wild type patterns. Thus, nine of 21 (43%) diepoxybutane-induced mutants are due to deletions ranging in size from approximately 50 base pairs to more than 8 kilobase pairs. Most of the deletions (seven of nine or 78%) are intragenic and less than 250 base pairs in size; it seems that most, if not all, affect coding rather than regulatory sequences.

Sign in / Sign up

Export Citation Format

Share Document