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

Genetics ◽  
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.

scholarly journals Non-mendelian female sterility in Drosophila melanogaster: variations of chromosomal contamination when caused by chromosomes of various inducer efficiencies

1978 ◽  
Vol 32 (2) ◽  
pp. 113-122 ◽  
Author(s):  
Alain Pélisson
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Recombination ◽  
Laboratory Strain ◽  
The Other ◽  
Female Sterility ◽  
Genetic Element ◽  
Specific Kind ◽  
Classical Genetic ◽  
Apparent Change

SUMMARYA quite specific kind of sterile F1 female, called SF females, arises only when females of strains denoted reactive are crossed with males of the other class (inducer). It was previously shown that this sterility results from a nucleocytoplasmic interaction between the maternal reactive cytoplasm and a factor, called I, which may be born by any one of the paternal chromosomes. In SF females, but not in their brothers, a varying proportion of reactive chromosomes are able to acquire irreversibly the I factor, independently of any classical genetic recombination with the inducer chromosome(s). During this process, called chromosomal contamination, the contaminating chromosome(s) do not undergo any apparent change. The present paper deals with the efficiency of both original inducer and contaminated chromosomes to yield a more or less intense SF sterility. The Otanu inducer laboratory strain contains at least two types of X chromosomes (called strong and weak) which differ genetically with respect to their inducer efficiency. Reactive third chromosomes were contaminated by these strong or weak X chromosomes and their inducer efficiencies compared. Results show that they are on average stronger when they have been contaminated by strong X chromosomes than when contaminated by weak ones. Such a correlation favours the hypothesis that chromosomal contamination is due to the insertion of some genetic element(s) into reactive chromosomes.

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

1985 ◽  
Vol 5 (10) ◽  
pp. 2567-2574 ◽  
Author(s):  
S Tsubota ◽  
M Ashburner ◽  
P Schedl
Keyword(s):  
Drosophila Melanogaster ◽  
The Other ◽  
P Element ◽  
Female Sterility ◽  
R Gene ◽  
Temporal Expression ◽  
Base Pairs ◽  
P Elements ◽  
Adult Females ◽  
Regulatory Mutations

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.

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

Genetics ◽  
1991 ◽  
Vol 129 (2) ◽  
pp. 371-383 ◽  
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.

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

Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 889-897
Author(s):  
S Y Tiong ◽  
D Nash
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Gene Product ◽  
Genetic Interaction ◽  
Chromosome Region ◽  
The Other ◽  
Purine Biosynthesis ◽  
Induced Mutations ◽  
Complementation Groups ◽  
Functional Complexity

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.

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

1985 ◽  
Vol 5 (10) ◽  
pp. 2567-2574
Author(s):  
S Tsubota ◽  
M Ashburner ◽  
P Schedl
Keyword(s):  
Drosophila Melanogaster ◽  
The Other ◽  
P Element ◽  
Female Sterility ◽  
R Gene ◽  
Temporal Expression ◽  
Base Pairs ◽  
P Elements ◽  
Adult Females ◽  
Regulatory Mutations

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.

Genetic analysis of enhancer of split, a locus involved in neurogenesis in Drosophila melanogaster.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 63-74
Author(s):  
A Ziemer ◽  
K Tietze ◽  
E Knust ◽  
J A Campos-Ortega
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Spontaneous Mutations ◽  
Genetic Complexity ◽  
Complementation Groups ◽  
Enhancer Of Split

Abstract Enhancer of split (E(spl)), one of the neurogenic loci of Drosophila, is uncovered by the deletion Df(3R)E(spl)(R-B251) with breakpoints at 96F8 and 96F13. We describe here the results of a genetic analysis of this chromosomal interval. Thirty-one mutations in genes of this region were recovered during various programs of mutagenesis. In addition, we included the spontaneous mutations E(spl)(D) and groucho (gro), which are known to map to this region, in our study. These 33 mutations define four lethal complementation groups, one of which includes E(spl)(D) and gro. Mutations of the E(spl) group behave as complementing and noncomplementing pseudoalleles, defining different functions. Alleles are classified according to their complementation behavior in two different ways: with respect to their viability as heterozygotes with other lethal alleles and with respect to gro and to E(spl)(D). The phenotypes of these mutations and the pattern of heteroallelic complementation speak in favor of a considerable genetic complexity of the E(spl) locus.

scholarly journals Genetic analysis of the Shaker gene complex of Drosophila melanogaster.

Genetics ◽  
1990 ◽  
Vol 125 (2) ◽  
pp. 383-398 ◽  
Author(s):  
A Ferrús ◽  
S Llamazares ◽  
J L de la Pompa ◽  
M A Tanouye ◽  
O Pongs
Keyword(s):  
Nervous System ◽  
Drosophila Melanogaster ◽  
Mutational Analysis ◽  
The Other ◽  
Functional Coupling ◽  
Gene Complex ◽  
Structural Locus ◽  
Functional Relationships ◽  
Complementation Groups ◽  
The Relationship

Abstract The Shaker complex (ShC) spans over 350 kb in the 16F region of the X chromosome. It can be dissected by means of aneuploids into three main sections: the maternal effect (ME), the viable (V) and the haplolethal (HL) regions. The mutational analysis of ShC shows a high density of antimorphic mutations among 12 lethal complementation groups in addition to 14 viable alleles. The complex is the structural locus of a family of potassium channels as well as a number of functions relevant to the biology of the nervous system. The constituents of ShC seem to be linked by functional relationships in view of the similarity of the phenotypes, antimorphic nature of their mutations and the behavior in transheterozygotes. We discuss the relationship between the genetic organization of ShC and the functional coupling of potassium currents with the other functions encoded in the complex.

scholarly journals A Cluster of Cuticle Protein Genes of Drosophila melanogaster at 65A: Sequence, Structure and Evolution

Genetics ◽  
1997 ◽  
Vol 147 (3) ◽  
pp. 1213-1224
Author(s):  
Jean-Philippe Charles ◽  
Carol Chihara ◽  
Shamim Nejad ◽  
Lynn M Riddiford
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Dna ◽  
Multiple Copy ◽  
Sequence Structure ◽  
Coding Regions ◽  
The Third ◽  
Genetic Complexity ◽  
Genes Encoding ◽  
Cuticle Protein ◽  
Cuticle Proteins

A 36-kb genomic DNA segment of the Drosophila melanogaster genome containing 12 clustered cuticle genes has been mapped and partially sequenced. The cluster maps at 65A 5-6 on the left arm of the third chromosome, in agreement with the previously determined location of a putative cluster encompassing the genes for the third instar larval cuticle proteins LCP5, LCP6 and LCP8. This cluster is the largest cuticle gene cluster discovered to date and shows a number of surprising features that explain in part the genetic complexity of the LCP5, LCP6 and LCP8 loci. The genes encoding LCP5 and LCP8 are multiple copy genes and the presence of extensive similarity in their coding regions gives the first evidence for gene conversion in cuticle genes. In addition, five genes in the cluster are intronless. Four of these five have arisen by retroposition. The other genes in the cluster have a single intron located at an unusual location for insect cuticle genes.

scholarly journals MUTATIONAL ANALYSIS OF THE REGION SURROUNDING THE 93D HEAT SHOCK LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1984 ◽  
Vol 106 (2) ◽  
pp. 249-265
Author(s):  
Jym Mohler ◽  
Mary Lou Pardue
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Mutational Analysis ◽  
Point Mutations ◽  
Γ Irradiation ◽  
Lethal Mutations ◽  
Complementation Groups ◽  
In Trans ◽  
Shock Locus ◽  
Shock Proteins

ABSTRACT The region containing subdivisions 93C, 93D and 93E on chromosome 3 of Drosophila melanogaster has been screened for visible and lethal mutations. Treatment with three mutagens, γ irradiation, ethyl methanesulfonate and diepoxybutane, has produced mutations that fall into 20 complementation groups, including the previously identified ebony locus. No point mutations affecting the heat shock locus in 93D were detected; however, a pair of deficiencies that overlap in the region of this locus was isolated. Flies heterozygous in trans for this pair of deficiencies are capable of producing all of the major heat shock puffs (except 93D) and the major heat shock proteins. In addition, these flies show recovery of normal protein synthesis following a heat shock.

Sign in / Sign up

Export Citation Format

Share Document