A genetic and molecular analysis of the 46C chromosomal region surrounding the FMRFamide neuropeptide gene in Drosophila melanogaster.

Abstract We have analyzed the FMRFamide neuropeptide gene region of Drosophila melanogaster. This gene maps to the 46C region of chromosome 2R; this interval previously was not well characterized. For this genetic and molecular analysis, we have used X-ray mutagenesis, EMS mutagenesis, and the recently reported local P element transposition method. We identified four overlapping deletions, two of which have proximal breakpoints that define a 50-60-kb region surrounding the FMRFamide gene in 46C. To this small region, we mapped three lethal complementation groups; 10 additional lethal complementation groups were mapped to more distal regions of 46CD. One of these groups corresponds to even-skipped, the other 12 are previously unidentified. Using various lines of evidence we excluded the possibility that FMRFamide corresponds to any of the three lethal complementation groups mapping to its immediate 50-60-kb vicinity. The positions of two of the three lethal complementation groups were identified with P elements using a local transposition scheme. The third lethal complementation group was excluded as being FMRFamide mutants by sequence analysis and by immunocytochemistry with proFMRFamide precursor-specific antibodies. This analysis has (1) provided a genetic map of the 46CD chromosomal region and a detailed molecular map of a portion of the 46C region and (2) provided additional evidence of the utility of local transposition for targeting nearby genes.

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

Genetics ◽

10.1093/genetics/119.2.377 ◽

1988 ◽

Vol 119 (2) ◽

pp. 377-390

Author(s):

D Gubb ◽

S McGill ◽

M Ashburner

Keyword(s):

Drosophila Melanogaster ◽

Chromosomal Region ◽

Molecular Level ◽

Hybrid Dysgenesis ◽

P Element ◽

Genomic Clones ◽

Element Insertion ◽

Chromosomal Deletions ◽

Complementation Groups ◽

Insertion Sites

Abstract 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.

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Molecular cloning and genetic analysis of the suppressor-of-white-apricot locus from Drosophila melanogaster

Molecular and Cellular Biology ◽

10.1128/mcb.7.7.2498-2505.1987 ◽

1987 ◽

Vol 7 (7) ◽

pp. 2498-2505

Author(s):

Z Zachar ◽

D Garza ◽

T B Chou ◽

J Goland ◽

P M Bingham

Keyword(s):

Drosophila Melanogaster ◽

Gene Transfer ◽

Genetic Analysis ◽

Developmental Stages ◽

Chromosomal Region ◽

Transcription Unit ◽

Complementation Group ◽

P Element ◽

Allele Specific ◽

New Mutations

We report genetic and molecular analysis of the suppressor-of-white-apricot [su(wa)] locus, one of several retrotransposon insertion allele-specific suppressor loci in Drosophila melanogaster. First, we isolated and characterized eight new mutations allelic to the original su(wa)1 mutation. These studies demonstrated that su(wa) mutations allelic to su(wa)1 affected a conventional D. melanogaster complementation group. Second, we cloned the chromosomal region containing the su(wa) complementation group by P element transposon tagging. The ca. 14-kilobase region surrounding the su(wa) complementation group contained five distinct transcription units, each with a different developmentally programmed pattern of expression. Third, we used a modified procedure for P-mediated gene transfer to identify the transcription unit corresponding to su(wa) by gene transfer. Fourth, we found that the presumptive su(wa) transcription unit produced a family of transcripts (ranging from ca. 3.5 to ca. 5.2 kilobases) in all developmental stages, tissue fractions, and cell lines we examined, suggesting that the gene is universally expressed.

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Disgenesia do híbrido em populações naturais de Drosophila melanogaster.

Ciência e Natura ◽

10.5902/2179460x27019 ◽

1999 ◽

Vol 21 (21) ◽

pp. 51 ◽

Cited By ~ 1

Author(s):

Chirlei Cintia Klein ◽

Liliana Essi ◽

Ronaldo Medeiros Golombieski ◽

Élgion Lúcio da Silva Loreto

Keyword(s):

Drosophila Melanogaster ◽

Molecular Analysis ◽

Natural Populations ◽

Rio Grande ◽

P Element ◽

Rio Grande Do Sul ◽

Genetic Traits ◽

P Elements ◽

Regulatory Capacity ◽

Element Activity

Hybrid dysgenesis has been defined as a remarkable syndrome of correlated genetic traits that are produced in some particular crosses between certain strains. The present study main objective was classify recently collected Drosophila melanogaster strains in relation to P element activity and regulatory capacity. Our results to natural populations trapped from Rio Grande do Sul, Brazil and Colombia shows that it fell on Q class, since all examinated strains has showed P elements by molecular analysis and low P activity. In the same way, these strains shows low susceptibility to P element action. The bigger values found in the colombian population are in agreement with the clinal hypothesis to P element activity.

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Transposable element-induced polygenic mutations in Drosophila melanogaster

Genetics Research ◽

10.1017/s0016672300027117 ◽

1987 ◽

Vol 49 (3) ◽

pp. 225-233 ◽

Cited By ~ 19

Author(s):

Trudy F. C. Mackay

Keyword(s):

Drosophila Melanogaster ◽

Transposable Element ◽

Quantitative Traits ◽

Natural Populations ◽

P Element ◽

Environmental Variance ◽

X Ray ◽

P Elements ◽

Very High ◽

Mutational Variance

SummaryP-element mutagenesis was used to contaminate M-strain second chromosomes with P elements. The effect of P-element transposition on abdominal and sternopleural bristle scores and on female productivity was deduced by comparing the distributions of these quantitative traits among the contaminated second-chromosome lines with a control population of M-strain second-chromosome lines free of P elements. Estimates of P-element-induced mutational variance, Vm, for these characters are very high, and mutational ‘heritabilities’ (Vm/Ve, the ratio of mutational variance to environmental variance) are of the same order as heritabilities of these traits from natural populations. P-element-induced mutational variance of abdominal bristle score is roughly two orders of magnitude greater than spontaneous and X-ray-induced Vm/Ve for this trait.

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The molecular organization of the Star/asteroid region, a region necessary for proper eye development in Drosophila melanogaster

Genome ◽

10.1139/g93-049 ◽

1993 ◽

Vol 36 (2) ◽

pp. 356-366 ◽

Cited By ~ 4

Author(s):

Theodore S. Higson ◽

June E. Tessiatore ◽

Sean A. Bennett ◽

Raymond C. Derk ◽

Michael A. Kotarski

Keyword(s):

Drosophila Melanogaster ◽

Molecular Data ◽

P Element ◽

Molecular Organization ◽

Induced Mutations ◽

Dna Breaks ◽

X Ray ◽

P Elements ◽

Large Deletions ◽

Endonuclease Mapping

The Star/asteroid (S/ast) region of Drosophila melanogaster has been cloned by P element transposon tagging using the snw chromosome as a source of defective P elements. In each mutation examined, the element integrated into the region was a 0.5-kb element from a region proximal to sn and not one of the head-to-head elements from the sn locus. Previously described spontaneous and X-ray induced mutations of S and ast were located on the molecular map by Southern analysis and restriction endonuclease mapping of genomic clones. S mutations are either large deletions of the cloned region or DNA breaks located near the P element insertions that cause ast mutations. Both S and ast mutations reduce the steady-state amounts of a 3.4-kb RNA. The molecular data, together with the phenotypic interactions observed for S and ast alleles, are consistent with the interpretation that S and ast mutations are lesions within the same gene or within genes that are functionally related.Key words: Drosophila, Star, asteroid, P elements.

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Molecular cloning and genetic analysis of the suppressor-of-white-apricot locus from Drosophila melanogaster.

Molecular and Cellular Biology ◽

10.1128/mcb.7.7.2498 ◽

1987 ◽

Vol 7 (7) ◽

pp. 2498-2505 ◽

Cited By ~ 6

Author(s):

Z Zachar ◽

D Garza ◽

T B Chou ◽

J Goland ◽

P M Bingham

Keyword(s):

Drosophila Melanogaster ◽

Gene Transfer ◽

Genetic Analysis ◽

Developmental Stages ◽

Chromosomal Region ◽

Transcription Unit ◽

Complementation Group ◽

P Element ◽

Allele Specific ◽

New Mutations

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P-Element Insertion Alleles of Essential Genes on the Third Chromosome of Drosophila melanogaster Correlation of Physical and Cytogenetic Maps in Chromosomal Region 86E-87F

Genetics ◽

10.1093/genetics/147.4.1697 ◽

1997 ◽

Vol 147 (4) ◽

pp. 1697-1722 ◽

Cited By ~ 1

Author(s):

Peter Deák ◽

Mahmoud M Omar ◽

Robert D C Saunders ◽

Margit Pál ◽

Orbán Komonyi ◽

...

Keyword(s):

Drosophila Melanogaster ◽

Genetic Maps ◽

P Element ◽

Drosophila Genome ◽

Induced Mutations ◽

Lethal Mutant ◽

P Elements ◽

Element Insertion ◽

The Third ◽

Complementation Groups

Abstract We have established a collection of 2460 lethal or semi-lethal mutant lines using a procedure thought to insert single P elements into vital genes on the third chromosome of Drosophila melanogaster. More than 1200 randomly selected lines were examined by in situ hybridization and 90% found to contain single insertions at sites that mark 89% of all lettered subdivisions of the Bridges' map. A set of chromosomal deficiencies that collectively uncover ~25% of the euchromatin of chromosome 3 reveal lethal mutations in 468 lines corresponding to 145 complementation groups. We undertook a detailed analysis of the cytogenetic interval 86E-87F and identified 87 P-element-induced mutations falling into 38 complementation groups, 16 of which correspond to previously known genes. Twenty-one of these 38 complementation groups have at least one allele that has a P-element insertion at a position consistent with the cytogenetics of the locus. We have rescued P elements and flanking chromosomal sequences from the 86E-87F region in 35 lines with either lethal or genetically silent P insertions, and used these as probes to identify cosmids and P1 clones from the Drosophila genome projects. This has tied together the physical and genetic maps and has linked 44 previously identified cosmid contigs into seven “super-contigs” that span the interval. STS data for sequences flanking one side of the P-element insertions in 49 lines has identified insertions in the αγ element at 87C, two known transposable elements, and the open reading frames of seven putative single copy genes. These correspond to five known genes in this interval, and two genes identified by the homology of their predicted products to known proteins from other organisms.

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P-Element Repression in Drosophila melanogaster by Variegating Clusters of P-lacZ-white Transgenes

Genetics ◽

10.1093/genetics/159.4.1631 ◽

2001 ◽

Vol 159 (4) ◽

pp. 1631-1642 ◽

Cited By ~ 4

Author(s):

Stéphane Ronsseray ◽

Antoine Boivin ◽

Dominique Anxolabéhère

Keyword(s):

Drosophila Melanogaster ◽

X Chromosome ◽

Maternal Effect ◽

P Element ◽

Lacz Reporter ◽

X Ray ◽

Subtelomeric Heterochromatin ◽

P Elements ◽

In Trans ◽

Element Activity

Abstract In Drosophila, clusters of P transgenes (P-lac-w) display a variegating phenotype for the w marker. In addition, X-ray-induced rearrangements of chromosomes bearing such clusters may lead to enhancement of the variegated phenotype. Since P-lacZ transgenes in subtelomeric heterochromatin have some P-element repression abilities, we tested whether P-lac-w clusters also have the capacity to repress P-element activity in the germline. One cluster (T-1), located on a rearranged chromosome (T2;3) and derived from a line bearing a variegating tandem array of seven P-lac-w elements, partially represses the dysgenic sterility (GD sterility) induced by P elements. This cluster also strongly represses in trans the expression of P-lacZ elements in the germline. This latter suppression shows a maternal effect. Finally, the combination of variegating P-lac-w clusters and a single P-lacZ reporter inserted in subtelomeric heterochromatic sequences at the X chromosome telomere (cytological site 1A) leads to strong repression of dysgenic sterility. These results show that repression of P-induced dysgenic sterility can be elicited in the absence of P elements encoding a polypeptide repressor and that a transgene cluster can repress the expression of a single homologous transgene at a nonallelic position. Implications for models of transposable element silencing are discussed.

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A hobo Transgene That Encodes the P-Element Transposase in Drosophila melanogaster: Autoregulation and Cytotype Control of Transposase Activity

Genetics ◽

10.1093/genetics/161.1.195 ◽

2002 ◽

Vol 161 (1) ◽

pp. 195-204 ◽

Cited By ~ 1

Author(s):

Michael J Simmons ◽

Kevin J Haley ◽

Craig D Grimes ◽

John D Raymond ◽

Jarad B Niemi

Keyword(s):

Drosophila Melanogaster ◽

Gonadal Dysgenesis ◽

P Element ◽

Hsp70 Gene ◽

Alternate Splicing ◽

Male And Female ◽

P Elements ◽

Male Germline ◽

Female Germline ◽

Transposase Expression

Abstract Drosophila were genetically transformed with a hobo transgene that contains a terminally truncated but otherwise complete P element fused to the promoter from the Drosophila hsp70 gene. Insertions of this H(hsp/CP) transgene on either of the major autosomes produced the P transposase in both the male and female germlines, but not in the soma. Heat-shock treatments significantly increased transposase activity in the female germline; in the male germline, these treatments had little effect. The transposase activity of two insertions of the H(hsp/CP) transgene was not significantly greater than their separate activities, and one insertion of this transgene reduced the transposase activity of P(ry+, Δ2-3)99B, a stable P transgene, in the germline as well as in the soma. These observations suggest that, through alternate splicing, the H(hsp/CP) transgene produces a repressor that feeds back negatively to regulate transposase expression or function in both the somatic and germline tissues. The H(hsp/CP) transgenes are able to induce gonadal dysgenesis when the transposase they encode has P-element targets to attack. However, this ability and the ability to induce P-element excisions are repressed by the P cytotype, a chromosomal/cytoplasmic state that regulates P elements in the germline.

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The Regulatory Properties of Autonomous Subtelomeric P Elements Are Sensitive to a Suppressor of variegation in Drosophila melanogaster

Genetics ◽

10.1093/genetics/143.4.1663 ◽

1996 ◽

Vol 143 (4) ◽

pp. 1663-1674 ◽

Cited By ~ 3

Author(s):

Stéphane Ronsseray ◽

Monique Lehmann ◽

Danielle Nouaud ◽

Dominique Anxolabéhère

Keyword(s):

Drosophila Melanogaster ◽

Genetic Recombination ◽

Natural Populations ◽

P Element ◽

Single Element ◽

Heterochromatin Protein 1 ◽

X Chromosomes ◽

P Elements ◽

Associated Sequences ◽

Regulatory Properties

Abstract Genetic recombination was used in Drosophila melanogaster to isolate P elements, inserted at the telomeres of X chromosomes (cytological site 1A) from natural populations, in a genetic background devoid of other P elements. We show that complete maternally inherited P repression in the germline (P cytotype) can be elicited by only two autonomous P elements at 1A and that a single element at this site has partial regulatory properties. The analysis of the surrounding chromosomal regions of the P elements at 1A shows that in all cases these elements are flanked by Telomeric Associated Sequences, tandemly repetitive noncoding sequences that have properties of heterochromatin. In addition, we show that the regulatory properties of P elements at 1A can be inhibited by some of the mutant alleles of the Su(var)205 gene and by a deficiency of this gene. However, the regulatory properties of reference P strains (Harwich and Texas 007) are not impaired by Su(var)205 mutations. Su(var)205 encodes Heterochromatin Protein 1 (HP1). These results suggest that the HP1 dosage effect on the P element properties is sitedependent and could involve the structure of the chromatin.

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