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M Ashburner

Publications and source records attributed to M Ashburner.

At least 91 records · Page 5Linked to original sources

The product of the Drosophila gene vasa is very similar to eukaryotic initiation factor-4A.

The vasa gene product of Drosophila melanogaster is required only in the female germ line. Progeny of females homozygous for vasa mutations lack posterior structures and pole cells. Isolation and characterization of vasa genomic and complementary DNA clones show that the transcript is abundant in the female germ line and early embryos only. The predicted amino acid sequence is very similar to those of the translation initiation factor eIF-4A and the human nuclear antigen p68.

Amino Acid Sequence↗

A selective screen to recover chromosomal deletions and duplications in Drosophila melanogaster.

A screen is described that will select for breakpoints within a restricted chromosomal region in Drosophila. The aberrations recovered can be used to construct chromosomes carrying synthetic duplications and deletions. Such chromosomes have applications in the mapping of complementation groups at both the genetic and molecular level. In particular, breakpoints recovered after P element hybrid dysgenesis tend to be associated with P element insertion sites. Such aberration breakpoints can be genetically mapped, as synthetic deletions, and then used as transposon-tagged sites for the recovery of genomic clones.

Animals↗

The molecular analyses of an antimorphic mutation of Drosophila melanogaster, Scutoid.

A dominant mutation of Drosophila melanogaster, Scutoid (Sco), acts as an antimorphic allele of the no-ocelli (noc) gene. In Sco the noc region has been transposed from 35B to 35D on chromosome arm 2L and the noc gene is now adjacent to snail (sna). Induced revertants of Sco are frequently mutant for sna or are aberrations broken very close to sna. A molecular analysis of the Sco chromosome has confirmed that noc is transposed and fused to the sna region. However, only part of the noc region is included within the transposition. The breakpoints of 19 chromosomally aberrant Sco revertants have been mapped at the molecular level. Fourteen of these breakpoints map to the noc region, spread over about 80 kb of DNA. The breakpoints of the remaining five are not within the DNA of the noc region and appear to map within sequences from the sna region. This has been shown directly for three of these, those associated with T(2;3)ScoR+13, In(2L)ScoR+24 and In(2L)ScoR+26. Thus mutation of either noc or sna, genes which are apparently unrelated in their wild-type functions, can revert the antimorphic phenotype of Sco.

Animals↗

Mutation of the Adh gene of Drosophila melanogaster containing an internal tandem duplication.

AdhnLA248 is an X-ray-induced mutation of the alcohol dehydrogenase gene of Drosophila melanogaster that lacks detectable ADH protein but is transcribed. The transcript of this mutant allele is longer than that of the wild type. This is because the mutation is a duplication of parts of the second and third exons of Adh and of the intron that normally separates them. The primary transcript of the mutant allele is processed by the removal of both of the identical copies of intron 3. This mutation presumably originated, in the haploid sperm, as two staggered single-stranded breaks that gave rise to the duplication as a consequence of replication after fertilization.

Alcohol Oxidoreductases↗

Molecular analysis of the Adh region of the genome of Drosophila melanogaster.

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.

Alcohol Oxidoreductases↗

P-element-induced control mutations at the r gene of Drosophila melanogaster.

The P-M hybrid dysgenesis system was used to produce five putative regulatory mutations at the rudimentary locus, r. All five mutations were the result of insertions at the 5' end of the gene, upstream of the proposed start of transcription. All of the mutants displayed a leaky wing phenotype, and four of the mutants showed an uncoupling of the wing and female-sterility phenotypes, suggesting that they altered the normal spatial and temporal expression of the r gene. Four of the insertions were P elements. The fifth insertion, which was larger than an intact P element, consisted of a small P element connected to non-P-element DNA. Two of the mutants produced very little r transcript in adult females and were clustered 80 to 150 base pairs upstream of the start of transcription. The other three mutants had higher levels of r transcript in adult females and were clustered 440 to 500 base pairs upstream of the start of transcription. All of the data suggest that the insertions are in a 5' noncoding region of the r gene involved in the control of its spatial and temporal expression.

Animals↗

The messenger RNA for alcohol dehydrogenase in Drosophila melanogaster differs in its 5' end in different developmental stages.

Alcohol dehydrogenase (EC 1.1.1.1) of Drosophila melanogaster is coded by a single structural gene, active in both larvae and adults. The major larval and adult transcripts of Adh differ in their 5'-untranslated regions. The major larval mRNA is about 1100 bases long, some 50 bases shorter than the major adult transcript. The 5' end of the larval mRNA is colinear with the genomic sequence immediately adjacent to the coding region, starting 70 base pairs (bp) upstream of the initiation codon. By contrast, the adult mRNA shares only 36 of its 123 5'-untranslated bases with the larval mRNA; the remaining 87 are encoded by a sequence 654 bp upstream. Both initiation sites are preceded by a TATA box some 24 bp upstream. The developmental specificity of Adh expression is seen, therefore, to have a counterpart in the specificity of transcription initiation at the two separate promoter regions.

Alcohol Dehydrogenase↗

The genetics of a small autosomal region of Drosophila melanogaster containing the structural gene for alcohol dehydrogenase. VI. Induced revertants of scutoid.

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.

Alcohol Oxidoreductases↗

The genetics of a small chromosome region of Drosophila melanogaster containing the structural gene for alcohol dehydrogenase. IV: scutoid, an antimorphic mutation.

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, 1(2)br35 and rd. The Sco phenotype is thought to result from a position effect at the newly created noc/l(2)br28 junction.

Alcohol Oxidoreductases↗

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.

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.

Alcohol Oxidoreductases↗

Cytogenetic and genetic mapping of a salivary gland secretion protein in Drosophila melanogaster.

The larval salivary gland secretion of Drosophila melanogaster is separated, by acid-urea polyacrylamide electrophoresis, into several different protein components. The genes specifying three of these had hitherto been located both genetically and cytogenetically, and shown to map close to sites that form prominent puffs in larval salivary gland chromosomes. A fourth component of the secretion (SGS-6), present in some, but not all, stocks of D. melanogaster, is shown to be under the control of a gene that maps to 3-42.0 and to bands 71 C1,2-71 F3,5. In those stocks that possess SGS-6 a puff is active in 71 C3-4 in Puff Stage 1, but not in older larvae. We conclude that this puff is the manifestation of a transcriptionally active Sgs-6 gene.

Animals↗

The control of ecdysterone-regulated puffs in Drosophila salivary glands.

The hormone ecdysterone induces a characteristic sequence of changes in puffing activity in the salivary gland chromosomes of Drosophila melanogaster. A few puffs are induced very rapidly by the hormone and a larger number are only active after a lag period of several hours. To study the interrelationship of the activities of these "early" and "late" puffs, genotypes aneuploid for two early puffs have been constructed. In the duplication genotype the early puffs are active for less time than in the euploids while in the deficient genotype they are active for a longer period. Under appropriate assay conditions duplication of the early puffs results in a greater and more rapid response of some, but not all, late puffs to the hormone. Deletion of the early puffs results in a delayed response of the same late puffs. These data support the idea that the early puffs are autoregulated and that their products control activity at some late puff sites.

Animals↗

The secretory proteins of the larval salivary gland of Drosophila melanogaster: Cytogenetic correlation of a protein and a puff.

The gene for a major salivary gland secretion protein (Sgs-1) in Drosophila melanogaster has been mapped to chromosome 2 between dp (13.0) and cl (16.5). In the late third instar larva, a puff forms in this region. This puff (25 B) regresses as the ecdysteroid concentration increases prior to puparium formation. Quantitative analysis of the secretory protein 1, showed that, when present in extra dose, region 25 B results in a significant elevation in its relative amount. This suggests that the structural gene for this protein is localized in this region and that its synthesis is directly correlated to the activity of the 25 B puff.

Animals↗