Genetic analysis of the adenosine3 (Gart) region of the second chromosome of Drosophila melanogaster.

Abstract The Gart gene of Drosophila melanogaster is known, from molecular biological evidence, to encode a polypeptide that serves three enzymatic functions in purine biosynthesis. It is located in polytene chromosome region 27D. One mutation in the gene (ade3(1)) has been described previously. We report here forty new ethyl methanesulfonate-induced mutations selected aga!nst a synthetic deficiency of the region from 27C2-9 to ++28B3-4. The mutations were characterized cytogenetically and by complementation analysis. The analysis apparently identifies 12 simple complementation groups. In addition, two segments of the chromosome exhibit complex complementation behavior. The first, the 28A region, gave three recessive lethals and also contains three known visible mutants, spade (spd), Sternopleural (Sp) and wingless (wg); a complex pattern of genetic interaction in the region incorporates both the new and the previously known mutants. The second region is at 27D, where seven extreme semilethal mutations give a complex complementation pattern that also incorporates ade3(1). Since ade3(1) is defective in one of the enzymatic functions encoded in the Gart gene, we assume the other seven also affect the gene. The complexity of the complementation pattern presumably reflects the functional complexity of the gene product. The phenotypic effects of the mutants at 27D are very similar to those described for ade2 mutations, which also interrupt purine biosynthesis.

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Genetic and molecular mapping of chromosome region 85A in Drosophila melanogaster.

Genetics ◽

10.1093/genetics/120.3.733 ◽

1988 ◽

Vol 120 (3) ◽

pp. 733-742

Author(s):

W K Jones ◽

J M Rawls

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Molecular Mapping ◽

Chromosome Region ◽

Chromosome Rearrangements ◽

Genetic Complementation ◽

Chromosomal Segment ◽

Molecular Map ◽

Molecular Studies ◽

Complementation Groups

Abstract Chromosome region 85A contains at least 12 genetic complementation groups, including the genes dhod, pink and hunchback. In order to better understand the organization of this chromosomal segment and to permit molecular studies of these genes, we have carried out a genetic analysis coupled with a chromosome walk to isolate the DNA containing these genes. Complementation tests with chromosomal deficiencies permitted unambiguous ordering of most of the complementation groups identified within the 85A region. Recombinant bacteriophage clones were isolated that collectively span over 120 kb of 85A DNA and these were used to produce a molecular map of the region. The breakpoint sites of a number of 85A chromosome rearrangements were localized on the molecular map, thereby delimiting regions of the DNA that contain the various genetic complementation groups.

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Genetic analysis of chromosome region 63 of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/128.4.763 ◽

1991 ◽

Vol 128 (4) ◽

pp. 763-775 ◽

Cited By ~ 1

Author(s):

A D Wohlwill ◽

J J Bonner

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Chromosome Region ◽

P Element ◽

Cytogenetic Mapping ◽

Lethal Mutations ◽

Complementation Groups

Abstract The salivary chromosome region including cytological division 63 of Drosophila melanogaster was genetically analyzed in order to (1) characterize this previously unstudied region and (2) attempt to isolate mutations in the hsp82 gene. Seven deletions which span this region were isolated, including four which remove the hsp82 gene. A Minute mutation was mapped to this region and this Minute was used to isolate duplications in the 63 region. These duplications map the Minute to 63B8-C1. F2 screens were initiated using deletions which remove the hsp82 gene. Over 15,000 chromosomes were screened, yielding 40 lethal mutations which comprise 14 complementation groups. Several of these mutations map outside the 63 region and appear to give second site interaction with the Minute locus. Four loci, including the Minute gene, are candidates for hsp82 mutations by cytogenetic mapping. These loci were tested for complementation with a P element carrying the hsp82 gene. However, none of the mutations was rescued.

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Genetic Analysis of a Y-Chromosome Region That Induces Triplosterile Phenotypes and Is Essential for Spermatid Individualization in Drosophila melanogaster

Genetics ◽

10.1093/genetics/155.1.179 ◽

2000 ◽

Vol 155 (1) ◽

pp. 179-189

Author(s):

Benjamin Timakov ◽

Ping Zhang

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Male Sterility ◽

Y Chromosome ◽

Fluorescent Probes ◽

Male Fertility ◽

Chromosome Region ◽

The Other ◽

Axonemal Dynein ◽

Dynein Arms

Abstract The heterochromatic Y chromosome of Drosophila melanogaster contains ~40 Mb of DNA but has only six loci mutable to male sterility. Region h1-h9 on YL, which carries the kl-3 and kl-5 loci, induces male sterility when present in three copies. We show that three separate segments within the region are responsible for the triplosterility and have an additive effect on male fertility. The triplosterile males displayed pleiotropic defects, beginning at early postmeiotic stages. However, the triplosterility was unaffected by kl-3 or kl-5 alleles. These data suggest that region h1-h9 is complex and may contain novel functions in addition to those of the previously identified kl-3 and kl-5 loci. The kl-3 and kl-5 mutations as well as deficiencies within region h1-h9 result in loss of the spermatid axonemal outer dynein arms. Examination using fluorescent probes showed that males deficient for h1-h3 or h4-h9 displayed a postmeiotic lesion with disrupted individualization complexes scattered along the spermatid bundle. In contrast, the kl-3 and kl-5 mutations had no effect on spermatid individualization despite the defect in the axonemes. These results demonstrate that region h1-h9 carries genetically separable functions: one required for spermatid individualization and the other essential for assembling the axonemal dynein arms.

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Genetics of Differences in Pheromonal Hydrocarbons Between Drosophila melanogaster and D. simulans

Genetics ◽

10.1093/genetics/143.1.353 ◽

1996 ◽

Vol 143 (1) ◽

pp. 353-364 ◽

Cited By ~ 3

Author(s):

Jerry A Coyne

Keyword(s):

Drosophila Melanogaster ◽

Sexual Dimorphism ◽

Genetic Analysis ◽

Species Difference ◽

The Other ◽

Chromosome 3 ◽

Apparent Effect ◽

The Third ◽

Hydrocarbon Profile ◽

The Right

Abstract Females of Drosophila melanogaster and its sibling species D. simulans have very different cuticular hydrocarbons, with the former bearing predominantly 7,11-heptacosadiene and the latter 7-tricosene. This difference contributes to reproductive isolation between the species. Genetic analysis shows that this difference maps to only the third chromosome, with the other three chromosomes having no apparent effect. The D. simulans alleles on the left arm of chromosome 3 are largely recessive, allowing us to search for the relevant regions using D. melanogaster deficiencies. At least four nonoverlapping regions of this arm have large effects on the hydrocarbon profile, implying that several genes on this arm are responsible for the species difference. Because the right arm of chromosome 3 also affects the hydrocarbon profile, a minimum of five genes appear to be involved. The large effect of the third chromosome on hydrocarbons has also been reported in the hybridization between D. simulans and its closer relative D. sechellia, implying either an evolutionaly convergence or the retention in D. sechllia of an ancestral sexual dimorphism.

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Genetic and molecular analysis of new female-specific lethal mutations at the gene Sxl of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/129.2.371 ◽

1991 ◽

Vol 129 (2) ◽

pp. 371-383 ◽

Cited By ~ 1

Author(s):

B Granadino ◽

M Torres ◽

D Bachiller ◽

E Torroja ◽

J L Barbero ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Point Mutation ◽

Dosage Compensation ◽

The Other ◽

Initial Activity ◽

Lethal Mutations ◽

Dna Insertion ◽

Complementation Groups ◽

Activity State ◽

Female Specific

Abstract We have isolated three female-specific lethal mutations at the gene Sex-lethal (Sxl): Sxlfb, Sxlfc and Sxlfd. We have carried out the complementation analysis between these mutations and other previously reported Sxlf mutations. It is possible to classify the alleles tested in this report into two complementation groups: the bc group defined by Sxlfb, and Sxlfc, and the LS group defined by SxlfLS. The other alleles tested affect both complementation groups albeit with different degrees. Contrary to what happens with mutations at the LS group, mutations at the bc group do not affect sex determination, nor late dosage compensation nor oogenesis. Both Sxlfb and Sxlfc present a DNA insertion of at least 5 kb between position -10 and -11 on the molecular map, within the fourth intron. On the contrary, Sxlfd, a strong mutation affecting all Sxl functions, is not associated to any detectable DNA alteration in Southern blots, so that it seems to be a "point" mutation. In agreement with their phenotypes, both Sxlfc/SxlfLS and Sxlfc homozygous female larvae express only the late Sxl transcripts characteristic of females, while females homozygous for SxlfLS express only the late Sxl transcripts characteristic of males. Moreover, Sxlfc presents a lethal synergistic interaction with mutations at either da or the X:A ratio, two signals that define the initial activity state of Sxl, while SxlfLS do not. These data suggest that the two complementation groups are related to the two sets of early and late Sxl transcripts, which are responsible for the early and late Sxl functions, respectively: Sxlfb and Sxlfc would affect the early functions and SxlfLS would affect the late Sxl functions.

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APPARENT GENETIC COMPLEXITY GENERATED BY DEVELOPMENTAL THRESHOLDS: THE APTEROUS LOCUS IN DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/110.2.281 ◽

1985 ◽

Vol 110 (2) ◽

pp. 281-297

Author(s):

Mary E Stevens ◽

Peter J Bryant

Keyword(s):

Drosophila Melanogaster ◽

Anterior Margin ◽

Wing Disc ◽

The Other ◽

Female Sterility ◽

Wing Margin ◽

Previous Conclusion ◽

Developmental Thresholds ◽

Genetic Complexity ◽

Complementation Groups

ABSTRACT Mutations at the apterous (ap) locus in Drosophila melanogaster give rise to three distinct phenotypes: aberrant wings, female sterility and precocious adult death. The wing phenotype includes five types of abnormality: blistering, deficiencies, duplications, high-order repetitions and transformation of structures. The mildest phenotype is seen with homozygous apblt animals which have either normal or slightly blistered wings. Most alleles produce, in the homozygote, a deficient wing in which part or all of the wing margin and wing blade is missing, but wing hinge and notum regions are normal. Animals hemizygous for each of 20 ap alleles, as well as apID/apXa heterozygotes, show duplication of parts of the notum associated with complete wing deficiency. Animals heterozygous for apc and the other tested ap alleles show repetitions of parts of the anterior wing margin, an engrailed-like transformation of posterior wing margin into anterior margin or both. Both apblt and apc show similar phenotypes in homozygotes and hemizygotes, yet both produce a less extreme phenotype than that of the other hemizygotes, suggesting that neither mutation causes loss of the entire ap + function. The 15 alleles that cause precocious death and female sterility occur in six complementation groups based on complementation for these phenotypes. This supports the previous conclusion that the effects of apterous mutations on the wing do not correlate with their effects on viability and fertility. We propose an explanation for the effects of apterous mutations on the wing in which quantitative reductions in the activity of gene product give rise to qualitatively different phenotypes because of different threshold requirements of the ap + function for critical events in wing disc development.

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GENETIC ANALYSIS OF THE ANTENNAPEDIA GENE COMPLEX (ANT-C) AND ADJACENT CHROMOSOMAL REGIONS OF DROSOPHILA MELANOGASTER. II. POLYTENE CHROMOSOME SEGMENTS 84A–84B1,2

Genetics ◽

10.1093/genetics/95.2.383 ◽

1980 ◽

Vol 95 (2) ◽

pp. 383-397

Author(s):

R A Lewis ◽

B T Wakimoto ◽

R E Denell ◽

T C Kaufman

Keyword(s):

Drosophila Melanogaster ◽

Genetic Analysis ◽

Normal Development ◽

Chromosome 3 ◽

Gene Complex ◽

Functional Sites ◽

Complementation Groups ◽

Chromosome Segments ◽

New Alleles ◽

New Mutations

ABSTRACT The existence of a gene complex in the proximal right arm of chromosome 3 of Drosophila melanogaster involved in the development of the head and thorax was originally suggested by the phenotypes of several dominant homoeotic mutations and their revertants. A screen for mutations utilizing Df(3R) AntpNS+R17 (proximally broken in salivary region 84B1,2) yielded, among 102 recovered mutations, 17 localized by deficiency mapping to the putative homoeotic cluster. These fell into four complementation groups, two of which were characterized by homoeotic phenotypes. To explore the limits of the Antennapedia gene complex (ANT-C) more proximally, a second screen has been undertaken utilizing Df(3R)Scr, a deficiency of 84A1-B1,2.——Of 2832 chromosomes screened, 21 bearing alterations localized to polytene interval 84A-84B1,2 have been recovered. Sixteen are recessive lethals, and five showing reduced viability display a visible phenotype in surviving individuals. Complementation and phenotypic analyses revealed four complementation groups proximal to those identified in the previous screen, including two new alleles of the recessive homoeotic mutation, proboscipedia (pb). Ten of the new mutations correspond to complementation groups defined previously in the Df(3R)AntpNS+R17 screen, four to the EbR11 group, two to the Scr group and four to the Antp group.——On the basis of the phenotypes of the 39 mutations localized to this region, plus their interactions with extant homoeotic mutations, we postulate that there are at least five functional sites comprising the ANT-C. Three have been demonstrated to he homoeotic in nature. The specific homoeotic transformations thus far observed suggest that these loci are critical for normal development of adult labial, maxillary and thoracic structures.

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The generation and genetic analysis of suppressors of lethal mutations in the Caenorhabditis elegans rol-3(V) gene.

Genetics ◽

10.1093/genetics/136.1.129 ◽

1994 ◽

Vol 136 (1) ◽

pp. 129-143 ◽

Cited By ~ 2

Author(s):

W B Barbazuk ◽

R C Johnsen ◽

D L Baillie

Keyword(s):

Caenorhabditis Elegans ◽

Genetic Analysis ◽

Genetic Interaction ◽

Temperature Sensitive ◽

Left Hand ◽

Larval Stages ◽

Allele Specific ◽

Complementation Groups ◽

Nematode Cuticle ◽

Developmental Role

Abstract The Caenorhabditis elegans rol-3(e754) mutation is a member of a general class of mutations affecting gross morphology, presumably through disruption of the nematode cuticle. Adult worms homozygous for rol-3(e754) exhibit rotation about their long axis associated with a left-hand twisted cuticle, musculature, gut and ventral nerve cord. Our laboratory previously isolated 12 recessive lethal alleles of rol-3. All these lethal alleles cause an arrest in development at either early or mid-larval stages, suggesting that the rol-3 gene product performs an essential developmental function. Furthermore, through the use of the heterochronic mutants lin-14 and lin-29, we have established that the expression of rol-3(e754)'s adult specific visible function is not dependent on the presence of an adult cuticle. In an attempt to understand rol-3's developmental role we sought to identify other genes whose products interact with that of rol-3. Toward this end, we generated eight EMS induced and two gamma irradiation-induced recessive suppressors of the temperature sensitive (ts) mid-larval lethal phenotype of rol-3(s1040ts). These suppressors define two complementation groups srl-1 II and srl-2 III; and, while they suppress the rol-3(s1040) lethality, they do not suppress the adult specific visible rolling phenotype. Furthermore, there is a complex genetic interaction between srl-2 and srl-1 such that srl-2(s2506) fails to complement all srl alleles tested. These results suggest that srl-1 and srl-2 may share a common function and, thus, possibly constitute members of the same gene family. Mutations in both srl-1 and srl-2 produce no obvious hermaphrodite phenotypes in the absence of rol-3(s1040ts); however, males homozygous for either srl-1 or srl-2 display aberrant tail morphology. We present evidence suggesting that the members of srl-2 are not allele specific with respect to their suppression of rol-3 lethality, and that rol-3 may act in some way to influence proper posterior morphogenesis. Finally, based on our genetic analysis of rol-3 and the srl mutations, we present a model whereby the wild-type products of the srl loci act in a concerted manner to negatively regulate the rol-3 gene.

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A Screen for Modifiers of Cyclin E Function in Drosophila melanogaster Identifies Cdk2 Mutations, Revealing the Insignificance of Putative Phosphorylation Sites in Cdk2

Genetics ◽

10.1093/genetics/155.1.233 ◽

2000 ◽

Vol 155 (1) ◽

pp. 233-244 ◽

Cited By ~ 1

Author(s):

Mary Ellen Lane ◽

Marion Elend ◽

Doris Heidmann ◽

Anabel Herr ◽

Sandra Marzodko ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Cyclin E ◽

S Phase ◽

Regulatory Subunit ◽

Phosphorylation Sites ◽

Induced Mutations ◽

Complementation Groups ◽

Higher Eukaryotes ◽

Eye Imaginal Disc ◽

Regulatory Significance

Abstract In higher eukaryotes, cyclin E is thought to control the progression from G1 into S phase of the cell cycle by associating as a regulatory subunit with cdk2. To identify genes interacting with cyclin E, we have screened in Drosophila melanogaster for mutations that act as dominant modifiers of an eye phenotype caused by a Sevenless-CycE transgene that directs ectopic Cyclin E expression in postmitotic cells of eye imaginal disc and causes a rough eye phenotype in adult flies. The majority of the EMS-induced mutations that we have identified fall into four complementation groups corresponding to the genes split ends, dacapo, dE2F1, and Cdk2(Cdc2c). The Cdk2 mutations in combination with mutant Cdk2 transgenes have allowed us to address the regulatory significance of potential phosphorylation sites in Cdk2 (Thr 18 and Tyr 19). The corresponding sites in the closely related Cdk1 (Thr 14 and Tyr 15) are of crucial importance for regulation of the G2/M transition by myt1 and wee1 kinases and cdc25 phosphatases. In contrast, our results demonstrate that the equivalent sites in Cdk2 play no essential role.

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Cytogenetic definition and morphogenetic analysis of Delta, a gene affecting neurogenesis in Drosophila melanogaster.

Genetics ◽

10.1093/genetics/118.2.235 ◽

1988 ◽

Vol 118 (2) ◽

pp. 235-245

Author(s):

A K Alton ◽

K Fechtel ◽

A L Terry ◽

S B Meikle ◽

M A Muskavitch

Keyword(s):

Nervous System ◽

Drosophila Melanogaster ◽

Genetic Analysis ◽

Inverse Correlation ◽

Small Interval ◽

Genetic Analyses ◽

The Third ◽

Complementation Groups ◽

Definition Of ◽

Morphogenetic Analysis

Abstract We have conducted a genetic analysis of a small interval of the third chromosome known to include Delta (Dl), a locus that affects the segregation of the ectoderm into neural and epidermal lineages during embryogenesis and the morphogenesis of some ectodermally derived structures, in Drosophila melanogaster. This analysis has led to the definition of seven independent complementation groups, one of which is Delta, within the interval extending from 91F6-13 to 92A2. Among the extant mutations in these seven loci, only mutations in Dl lead to the so-called neurogenic phenotype: hypertrophy of the nervous system and reduction of the epidermis. Combined cytogenetic and genetic analyses allow us to define absolute proximal (91F5-92A1) and distal (92A2) cytogenetic limits for the Dl locus. We have isolated hypomorphic and amorphic alleles of Dl and find that, for any given allele, there is an inverse correlation between neural hypertrophy and epidermal reduction in embryos and a direct correlation between the severity of embryonic phenotypes in mutant homozygotes and hemizygotes and the imaginal phenotype in heterozygous adults.

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