THE GENETICS OF A SMALL AUTOSOMAL REGION OF DROSOPHILA MELANOGASTER CONTAINING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. III. HYPOMORPHIC AND HYPERMORPHIC MUTATIONS AFFECTING THE EXPRESSION OF HAIRLESS

ABSTRACT A lethal locus (1(2)br7;35B6-10), near Adh on chromosome arm 2L of D. melanogaster, is identified with Plunkett's dominant suppressor of Hairless (H). Of eight new alleles, seven act as dominant suppressors of H, the eighth is a dominant enhancer of H. One of the suppressor alleles is both a leaky lethal and a weak suppressor of H. Confirming Nash (1970), deletions of 1(2)br7 are dominant suppressors, and duplications are dominant enhancers of H. A simple model is proposed to account for the interaction of 1(2)br7 and H, assuming that amorphic (or hypomorphic) alleles of l(2)br7 suppress H and that hypermorphic alleles enhance H.

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THE GENETICS OF A SMALL AUTOSOMAL REGION OF DROSOPHILA MELANOGASTER, INCLUDING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. V. CHARACTERIZATION OF X-RAY-INDUCED Adh NULL MUTATIONS

Genetics ◽

10.1093/genetics/102.3.421 ◽

1982 ◽

Vol 102 (3) ◽

pp. 421-435

Author(s):

M Ashburner ◽

C S Aaron ◽

S Tsubota

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

End Points ◽

X Ray ◽

Autosomal Region ◽

Nonrandom Distribution ◽

Chromosome Arm ◽

Break Points

ABSTRACT Of 31 X-ray-induced and 2 spontaneous Adh null mutations selected for resistance to pentenol (Aaron 1979), 21 are deletions, including Adh and one or more neighboring loci. By contrast, none of 13 EMS-induced Adhn mutations are deletions. On average, the size of these X-ray-induced deletions is shorter than that of 12 formaldehyde-induced Adhn deletions (O'Donnell, Mandell, Krauss and Sofer 1977). Both the X-ray- and formaldehyde-induced deletions show a nonrandom distribution of break points in region 34D to 35D of chromosome arm 2L. Some of the deletions display particular genetic properties associated with one of their end points.

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THE GENETICS OF A SMALL AUTOSOMAL REGION OF DROSOPHILA MELANOGASTER CONTAINING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. II. LETHAL MUTATIONS IN THE REGION

Genetics ◽

10.1093/genetics/92.1.133 ◽

1979 ◽

Vol 92 (1) ◽

pp. 133-149

Author(s):

R C Woodruff ◽

M Ashburner

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

Small Region ◽

Lethal Mutations ◽

Autosomal Region ◽

Chromosome Arm ◽

Genetic Features ◽

Complementation Groups ◽

Ectopic Pairing

ABSTRACT Forty-seven lethal mutations and alleles of nine visible loci (including alcohol dehydrogenase) have been mapped by both deficiency mapping and, in most cases, by recombination mapping to a small region (34D-35C) of chromosome arm 2L of Drosophila melanogaster. The lethals fall into approximately 21 complementation groups, and we estimate that the total number of lethal plus visible complementation groups within the 34-band deficiency, Df(2L)64j, is approximately 34, a remarkable numerical coincidence. The possible genetic significance of this coincidence is discussed. Lethals mapping close to the structural gene for alcohol dehydrogenase, both distally and proximally, have been identified and will be used for the construction of selective crosses for the study of exchange within this locus. Despite many abnormal cytological features (e.g., ectopic pairing, weak points) region 35 of chromosome arm 2L does not display any unusual genetic features; indeed, in terms of the aniount of recombination per band and the average map distance between adjacent loci, this region is similar to that between zeste and white on the X chromosome.

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THE GENETICS OF A SMALL AUTOSOMAL REGION OF DROSOPHILA MELANOGASTER CONTAINING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. VI. INDUCED REVERTANTS OF SCUTOID

Genetics ◽

10.1093/genetics/104.3.405 ◽

1983 ◽

Vol 104 (3) ◽

pp. 405-431

Author(s):

M Ashburner ◽

C Detwiler ◽

S Tsubota ◽

R C Woodruff

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

Chromosome Aberrations ◽

Dominant Mutation ◽

Autosomal Region ◽

Genetic Complexity ◽

Chromosome Arm ◽

Mutant Chromosome

ABSTRACT Twenty-six induced revertants of Scutoid (Sco), a dominant mutation of Drosophila melanogaster, have been characterized genetically. Sco is an unusual mutation, involving two small reciprocal transpositions within the region 35A4 to 35C5 of chromosome arm 2L. One of these transpositions juxtaposes the noc and l(2)br28 loci. We suggested previously that the Sco phenotype results from the "fusion" of noc and l(2)br28. In support of this idea we now show that 23 of 26 revertants of Sco are noc -, indeed the majority are either chromosome aberrations broken between noc and l(2)br28 or deletions of these loci from the mutant chromosome. However, some revertants of Sco are rather more complex, and their properties suggest an interaction between the pu-noc and l(2)br28-l(2)br37 regions of chromosome arm 2L and also demonstrate the genetic complexity of the el-noc region.

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The genetics of a small autosomal region of Drosophila melanogaster containing the structural gene for alcohol dehydrogenase. VII. Characterization of the region around the snail and cactus loci.

Genetics ◽

10.1093/genetics/126.3.679 ◽

1990 ◽

Vol 126 (3) ◽

pp. 679-694 ◽

Cited By ~ 1

Author(s):

M Ashburner ◽

P Thompson ◽

J Roote ◽

P F Lasko ◽

Y Grau ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

Maternal Effect ◽

Autosomal Region ◽

Complex Interactions ◽

Chromosome Arm ◽

Genetic Interval ◽

Snail Gene

Abstract The genetic interval 35C to 36A on chromosome arm 2L of Drosophila melanogaster has been saturated for mutations with visible or lethal phenotypes. 38 loci have been characterized, including several maternal-effect lethals (vasa, Bic-C, chiffon, cactus and cornichon) and several early embryonic lethals, including snail and fizzy. About 130 deletions have been used to order these loci. Complex interactions between mutant alleles have been uncovered in the immediate genetic environs of the snail gene, as has further evidence for an interaction between this region and that including the nearby genes no-ocelli and elbow.

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THE GENETICS OF A SMALL CHROMOSOME REGION OF DROSOPHILA MELANOGASTER CONTAINING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. IV: SCUTOID, AN ANTIMORPHIC MUTATION

Genetics ◽

10.1093/genetics/102.3.401 ◽

1982 ◽

Vol 102 (3) ◽

pp. 401-420

Author(s):

M Ashburner ◽

S Tsubota ◽

R C Woodruff

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

Chromosome Region ◽

Position Effect ◽

Small Chromosome ◽

Deletion Mapping ◽

Dominant Mutation ◽

Chromosome Arm ◽

The Right

ABSTRACT Exchange mapping locates the dominant mutation Scutoid to the right of Adh on chromosome arm 2L of D. melanogaster. However, deletion mapping indicates that Sco is to the left of Adh. The phenotype of Sco is sensitive to mutation, or deletion, of noc + and of three genes, el, l(2)br22, and l(2)br29 mapping immediately distal to noc. The four contiguous loci, el, l(2)br22, l(2)br29 and noc, although separable by deletion end points, interact, because certain (or all) alleles of these four loci show partial failure of complementation, or even negative complementation. The simplest hypothesis is that Sco is a small reciprocal transposition, the genes noc, osp, and Adh exchanging places with three genes normally mapping proximal to them: l(2)br34, l(2)br35 and rd. The Sco phenotype is thought to result from a position effect at the newly created noc/l(2)br28 junction.

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THE GENETICS OF A SMALL AUTOSOMAL REGION OF DROSOPHILA MELANOGASTER CONTAINING THE STRUCTURAL GENE FOR ALCOHOL DEHYDROGENASE. I. CHARACTERIZATION OF DEFICIENCIES AND MAPPING OF ADH AND VISIBLE MUTATIONS

Genetics ◽

10.1093/genetics/92.1.117 ◽

1979 ◽

Vol 92 (1) ◽

pp. 117-132

Author(s):

R C Woodruff ◽

M Ashburner

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Polytene Chromosome ◽

Structural Gene ◽

Chromosome Region ◽

Autosomal Region ◽

Gene Coding ◽

Chromosome Bands ◽

Negative Phenotype

ABSTRACT The position of the structural gene coding for alcohol dehydrogenase (ADH) in Drosophila melanoguster has been shown to be within polytene chromosome bands 35B1 and 35B3, most probably within 35B2. The genetic and cytological properties of twelve deficiencies in polytene chromosome region 34-35 have been characterized, eleven of which include Adh. Also mapped cytogenetically are seven other recessive visible mutant loci. Flies heterozygous for overlapping deficiencies that include both the Adh locus and that for the outspread mutant (osp: a recessive wing phenotype) are homozygous viable and show a complete ADH negative phenotype and strong osp phenotype. These deficiencies probably include two polytene chromosome bands, 35B2 and 35B3.

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Alcohol dehydrogenase activity in Drosophila melanogaster: a quantitative character

Genetics Research ◽

10.1017/s0016672300015871 ◽

1975 ◽

Vol 26 (1) ◽

pp. 81-93 ◽

Cited By ~ 39

Author(s):

R. D. Ward

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Dehydrogenase Activity ◽

Structural Gene ◽

Genetic Background ◽

Quantitative Character ◽

Alcohol Dehydrogenase Activity ◽

Activity Modifiers ◽

Selection For ◽

Adh Activity

SUMMARYAlcohol dehydrogenase activity in Drosophila melanogaster may be considered as a quantitative character, since it shows many features typically associated with such traits. Although strains with the electrophoretically fast phenotype generally have activities greater than those with the slow phenotype, presumably reflecting differences in the nucleotide sequences of the structural alleles, within each electrophoretic class there is considerable variation in activity. The expression of the structural gene, in terms of ADH activity, is to some extent regulated by its genetic background. Strains homozygous for particular structural alleles respond to divergent directional selection for ADH activity. Modifiers have been located to the X, second and third chromosomes.

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GENETIC CONTROL OF Adh EXPRESSION IN DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/105.4.921 ◽

1983 ◽

Vol 105 (4) ◽

pp. 921-933

Author(s):

G Maroni ◽

C C Laurie-Ahlberg

Keyword(s):

Drosophila Melanogaster ◽

Alcohol Dehydrogenase ◽

Genetic Mapping ◽

Genetic Control ◽

Structural Gene ◽

Cis Acting ◽

Multiple Loci ◽

Natural Variants ◽

The Difference ◽

Different Levels

ABSTRACT Natural variants displaying different levels of expression of the gene for alcohol dehydrogenase (Adh) were subjected to genetic mapping experiments. The strains studied carry one of the two common electrophoretic forms of the enzyme. The difference among Adh - fast strains appears to be due to multiple loci with trans-acting effects. Differences among Adh - slow strains are due to modifiers or quantitative sites located very close to the structural gene (less than 0.05 map unit) or part of it. The modifiers detected in the Adhs strains seem to operate only on the structural allele in the cis-position.—A modifier that affects the ratio of ADH levels in larvae and adults was also detected in the Adhs strains. This modifier is also closely linked to Adh and is cis-acting.

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Molecular and Recombinational Mapping of Mutations in the Ace Locus of Drosophila melanogaster

Genetics ◽

10.1093/genetics/117.3.487 ◽

1987 ◽

Vol 117 (3) ◽

pp. 487-502

Author(s):

Rodney N Nagoshi ◽

William M Gelbart

Keyword(s):

Drosophila Melanogaster ◽

Fine Structure ◽

Structural Gene ◽

Molecular Analysis ◽

Restriction Site ◽

Deletion Mapping ◽

Cdna Sequences ◽

Chromosome Arm ◽

Recombinational Analysis ◽

Ace Activity

ABSTRACT The Ace locus in Drosophila melanogaster is known to be the structural gene for acetylcholinesterase. Ace is located in a region of chromosome arm 3R which has been subjected to intensive genetic and molecular analysis. Previous deletion mapping studies have identified a 40-kb region within which the Ace gene resides. This report focuses on the further localization of Ace within this 40-kb interval. Within this region, selective fine structure recombinational analysis was employed to localize three recessive Ace lethals relative to unselected restriction site variations. These three mutations fall into a segment of 7 kb within the Ace interval. Fine structure recombinational analysis was also used to confirm that the Ace - phenotype of one deletion, Df(3R)AceHD1, co-segregated with the molecular deletion. This deletion does not fully remove Ace activity, but it behaves as a recessive Ace lethal. Df(3R)AceHD1is the most distal Ace lesion identified and indicates that the Ace locus must extend at least 16 kb. Several poly(A)transcripts are detectable in the region defined by the Ace lesions. The position and extent of the Ace locus, as well as the types of transcripts found, is consistent with the recent findings which identified Torpedo-AChE homologous cDNA sequences in this region.

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GENETIC VARIATION IN THE EXPRESSION OF ADH IN DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/101.3-4.431 ◽

1982 ◽

Vol 101 (3-4) ◽

pp. 431-446

Author(s):

G Maroni ◽

C C Laurie-Ahlberg ◽

D A Adams ◽

A N Wilton

Keyword(s):

Drosophila Melanogaster ◽

Genetic Variation ◽

Alcohol Dehydrogenase ◽

Structural Gene ◽

Alimentary Canal ◽

Fat Body ◽

Natural Populations ◽

Enzyme Protein ◽

Fat Bodies ◽

Highly Correlated

ABSTRACT Several chromosomes derived from natural populations have been identified that affect the expression of alcohol dehydrogenase (ADH) . Second chromosomes, which also carry the structural gene Adh, show a great deal of polymorphism of genetic elements that determine how much enzyme protein accumulates. The level of enzyme was measured in third instar larvae, 6-to-8-day-old males and in larval fat bodies and alimentary canals. In general, activities in the different organs and stages are highly correlated with one another. One line was found, however, in which the ADH level in the fat body is more than twice the level one would expect on the basis of the activity in alimentary canal. We have also found evidence of third-chromosome elements that affect the level of ADH.

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