Meiotic recombination is suppressed near the histone-defined border of euchromatin and heterochromatin on chromosome 2L of Drosophila melanogaster

Genome ◽  
2016 ◽  
Vol 59 (4) ◽  
pp. 289-294 ◽  
Author(s):  
Alistair B. Coulthard ◽  
Rhodri W. Taylor-Kamall ◽  
Graham Hallson ◽  
Anna Axentiev ◽  
Don A. Sinclair ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Histone Modifications ◽  
Meiotic Recombination ◽  
Pericentric Heterochromatin ◽  
P Element ◽  
White Gene ◽  
Chromosomal Proteins ◽  
Chromatin States ◽  
Genetic Property ◽  
Element Insertion

In Drosophila melanogaster, the borders between pericentric heterochromatin and euchromatin on the major chromosome arms have been defined in various ways, including chromatin-specific histone modifications, the binding patterns of heterochromatin-enriched chromosomal proteins, and various cytogenetic techniques. Elucidation of the genetic properties that independently define the different chromatin states associated with heterochromatin and euchromatin should help refine the boundary. Since meiotic recombination is present in euchromatin, but absent in heterochromatin, it constitutes a key genetic property that can be observed transitioning between chromatin states. Using P element insertion lines marked with a su(Hw) insulated mini-white gene, meiotic recombination was found to transition in a region consistent with the H3K9me2 transition observed in ovaries.

scholarly journals hobo enhancer trapping mutagenesis in Drosophila reveals an insertion specificity different from P elements.

Genetics ◽  
1993 ◽  
Vol 135 (4) ◽  
pp. 1063-1076 ◽  
Author(s):  
D Smith ◽  
J Wohlgemuth ◽  
B R Calvi ◽  
I Franklin ◽  
W M Gelbart
Keyword(s):  
Drosophila Melanogaster ◽  
Transposable Element ◽  
Enhancer Trap ◽  
P Element ◽  
Present Evidence ◽  
P Elements ◽  
Element Insertion ◽  
Enhancer Trapping ◽  
Indispensable Tool

Abstract P element enhancer trapping has become an indispensable tool in the analysis of the Drosophila melanogaster genome. However, there is great variation in the mutability of loci by these elements such that some loci are relatively refractory to insertion. We have developed the hobo transposable element for use in enhancer trapping and we describe the results of a hobo enhancer trap screen. In addition, we present evidence that a hobo enhancer trap element has a pattern of insertion into the genome that is different from the distribution of P elements in the available database. Hence, hobo insertion may facilitate access to genes resistant to P element insertion.

Molecular organization and expression of the genetic locus glued in Drosophila melanogaster

1986 ◽  
Vol 6 (3) ◽  
pp. 833-841
Author(s):  
A Swaroop ◽  
J W Sun ◽  
M L Paco-Larson ◽  
A Garen
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Function ◽  
Genetic Locus ◽  
Insertion Site ◽  
Lethal Effect ◽  
P Element ◽  
Molecular Organization ◽  
General Distribution ◽  
Element Insertion ◽  
Mutant Phenotypes

The Glued locus of Drosophila melanogaster is genetically defined as the functional unit which is affected by the dominant Glued mutation Gl. Genomic DNA was cloned from the region of the Glued locus, at 70C2 on chromosome 3, by using a P element insertion in the region as a molecular marker. Three genes encoding polyadenylated transcripts were detected within a 30-kilobase span of the cloned DNA. The gene nearest the P element insertion site was identified as a Glued gene on the basis of alterations in its DNA and encoded transcript associated with the Gl mutation and with reversions of Gl which eliminate the dominant effect by inactivation of the mutant allele. Expression of the wild-type Gl+ gene is temporally regulated during development; the amount of the encoded transcript is highest in the embryonic stage, decreasing in the first and second larval instars, and then increasing in the third instar and pupal stages. There is a maternal contribution of the Gl+ transcript to the embryo, which probably accounts for the maternal lethal effect of Glued mutations on early development. In situ hybridizations of Gl+ DNA to RNA in tissue sections showed that the Gl+ transcript is present in virtually all tissues of the embryo, late larva, and pupa. The general distribution of this transcript is consistent with genetic evidence indicating that the Glued locus controls a generally essential cell function (P. J. Harte and D. R. Kankel, Genetics 101:477-501, 1982). Different Glued mutations produce distinct phenotypic effects, including adults with severe visual defects, larvae lacking imaginal discs, and early lethality. These diverse mutant phenotypes are discussed in terms of quantitative changes in the Glued function. Closely adjacent to Gl+ is another gene which is transcribed in a divergent direction and expressed coordinately with Gl+ throughout Drosophila development. It remains to be determined whether this gene is also involved with the Glued function.

scholarly journals A particular P-element insertion is correlated to the P-induced hybrid dysgenesis repression in Drosophila melanogaster

1992 ◽  
Vol 60 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Dominique Higuet ◽  
Dominique Anxolabéhére ◽  
Danielle Nouaud
Keyword(s):  
Drosophila Melanogaster ◽  
Promoter Activity ◽  
Hybrid Dysgenesis ◽  
P Element ◽  
P Elements ◽  
Element Insertion ◽  
Element Number

SummaryTransposable P elements in Drosophila melanogaster cause hybrid dysgenesis if their mobility is not repressed. The ability to regulate the dysgenic activity of the P elements depends on several mechanisms, one of which hypothesized that a particular deleted P element (the KP element) results in a non-susceptibility which is biparentally transmitted. In this study totally nonsusceptible lines, and susceptible lines containing exclusively KP elements (IINS2 line and IIS2 line) were isolated from a M' strain. We show that non-susceptibility is correlated with a particular insertion of one KP element located at the cytological site 47D1. The repression ability of the GD sterility is determined by a recessive chromosomal factor, and cannot be due to the KP-element number. Here the repression of the P mobility is associated with reduction of the P transcripts and the inhibition of P promoter activity.

scholarly journals Molecular cloning of suppressor of sable, a Drosophila melanogaster transposon-mediated suppressor.

1986 ◽  
Vol 6 (5) ◽  
pp. 1520-1528 ◽  
Author(s):  
D Y Chang ◽  
B Wisely ◽  
S M Huang ◽  
R A Voelker
Keyword(s):  
Drosophila Melanogaster ◽  
Dna Sequences ◽  
Insertion Site ◽  
Hybrid Dysgenesis ◽  
P Element ◽  
Dna Transformation ◽  
Wild Type ◽  
Induced Mutations ◽  
X Ray ◽  
Element Insertion

A hybrid dysgenesis-induced allele [su(s)w20] associated with a P-element insertion was used to clone sequences from the su(s) region of Drosophila melanogaster by means of the transposon-tagging technique. Cloned sequences were used to probe restriction enzyme-digested DNAs from 22 other su(s) mutations. None of three X-ray-induced or six ethyl methanesulfonate-induced su(s) mutations possessed detectable variation. Seven spontaneous, four hybrid dysgenesis-induced, and two DNA transformation-induced mutations were associated with insertions within 2.0 kilobases (kb) of the su(s)w20 P-element insertion site. When the region of DNA that included the mutational insertions was used to probe poly(A)+ RNAs, a 5-kb message was detected in wild-type RNA that was present in greatly reduced amounts in two su(s) mutations. By using strand-specific probes, the direction of transcription of the 5-kb message was determined. The mutational insertions lie in DNA sequences near the 5' end of the 5-kb message. Three of the seven spontaneous su(s) mutations are associated with gypsy insertions, but they are not suppressible by su(Hw).

scholarly journals Local transposition of P elements in Drosophila melanogaster and recombination between duplicated elements using a site-specific recombinase.

Genetics ◽  
1994 ◽  
Vol 137 (2) ◽  
pp. 551-563 ◽  
Author(s):  
K G Golic
Keyword(s):  
Drosophila Melanogaster ◽  
Sister Chromatid ◽  
P Element ◽  
White Gene ◽  
Direct Repeats ◽  
Site Specific ◽  
P Elements ◽  
Dicentric Chromosomes ◽  
A Site ◽  
Different Levels

Abstract The transposase source delta 2-3(99B) was used to mobilize a P element located at sites on chromosomes X, 2 and 3. The transposition event most frequently recovered was a chromosome with two copies of the P element at or near the original site of insertion. These were easily recognized because the P element carried a hypomorphic white gene with a dosage dependent phenotype; flies with two copies of the gene have darker eyes than flies with one copy. The P element also carried direct repeats of the recombination target (FRT) for the FLP site-specific recombinase. The synthesis of FLP in these flies caused excision of the FRT-flanked white gene. Because the two white copies excised independently, patches of eye tissue with different levels of pigmentation were produced. Thus, the presence of two copies of the FRT-flanked white gene could be verified. When the P elements lay in the same orientation, FLP-mediated recombination between the FRTs on separated elements produced deficiencies and duplications of the flanked region. When P elements were inverted, the predominant consequence of FLP-catalyzed recombination between the inverted elements was the formation of dicentric chromosomes and acentric fragments as a result of unequal sister chromatid exchange.

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

Genetics ◽  
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.

scholarly journals Homology Requirements for Targeting Heterologous Sequences During P-Induced Gap Repair in Drosophila melanogaster  1

Genetics ◽  
1997 ◽  
Vol 147 (2) ◽  
pp. 689-699 ◽  
Author(s):  
Tammy Dray ◽  
Gregory B Gloor
Keyword(s):  
Drosophila Melanogaster ◽  
Point Mutations ◽  
Double Strand Breaks ◽  
Yellow Gene ◽  
P Element ◽  
White Gene ◽  
Base Pairs ◽  
Strand Breaks ◽  
Distal Point ◽  
White Locus

The effect of homology on gene targeting was studied in the context of P-element-induced double-strand breaks at the white locus of Drosophila melanogaster. Double-strand breaks were made by excision of P-whd, a P-element insertion in the white gene. A nested set of repair templates was generated that contained the 8 kilobase (kb) yellow gene embedded within varying amounts of white gene sequence. Repair with unlimited homology was also analyzed. Flies were scored phenotypically for conversion of the yellow gene to the white locus. Targeting of the yellow gene was abolished when all of the 3′ homology was removed. Increases in template homology up to 51 base pairs (bp) did not significantly promote targeting. Maximum conversion was observed with a construct containing 493 bp of homology, without a significant increase in frequency when homology extended to the tips of the chromosome. These results demonstrate that the homology requirements for targeting a large heterologous insertion are quite different than those for a point mutation. Furthermore, heterologous insertions strongly affect the homology requirements for the conversion of distal point mutations. Several aberrant conversion tracts, which arose from templates that contained reduced homology, also were examined and characterized.

scholarly journals The fitness consequences of P element insertion in Drosophila melanogaster

1988 ◽  
Vol 52 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Walter F. Eanes ◽  
Cedric Wesley ◽  
Jody Hey ◽  
David Houle ◽  
James W. Ajioka
Keyword(s):  
Drosophila Melanogaster ◽  
Relative Number ◽  
African Population ◽  
P Element ◽  
Insertion Event ◽  
Element Insertion ◽  
Lethal Mutations ◽  
Fitness Consequences ◽  
Per Se

SummaryIn this study we estimate the frequency at which P-element insertion events, as identified by in situ hybridization, generate lethal and mild viability mutations. The frequency of lethal mutations generated per insertion event was 0·004. Viability dropped an average of 1% per insertion event. Our results indicate that it is deletions and rearrangements resulting from the mobilization of P elements already in place and not the insertions per se that cause the drastic effects on viability and fitness observed in most studies of P–M dysgenesis-derived mutations. Elements of five other families (I, copia, 412, B104, and gypsy) were not mobilized in these crosses. Finally, we contrast the density of P elements on the X chromosome with the density on the four autosomal arms in a collection of thirty genomes from an African population. The relative number of P elements on the X chromosome is too high to be explained by either a hemizygous selection or a neutrality model. The possible reasons for the failure to detect selection are discussed.

scholarly journals Mapping and characterization of P-element-induced mutations at quantitative trait loci in Drosophila melanogaster

1993 ◽  
Vol 61 (3) ◽  
pp. 177-193 ◽  
Author(s):  
Chaoqiang Lai ◽  
Trudy F. C. Mackay
Keyword(s):  
Drosophila Melanogaster ◽  
Physical Mapping ◽  
Hybridization Analysis ◽  
P Element ◽  
Complementation Test ◽  
Induced Mutations ◽  
Element Insertion ◽  
Bristle Number ◽  
Chromosomal Bands

SummaryX chromosomes derived from crosses of inbred P and M Drosophila melanogaster strains that had extreme effects on abdominal and/or sternopleural bristle number in males, were further analyzed to determine their effects in females and to map the loci at which the mutations occurred. Seven lines that had on average 3.9 fewer sternopleural bristles than wildtype in males had average homozygous sternopleural bristle effects of −2·2. The bristle effects were partially recessive, with an average degree of dominance of −0·60. Physical mapping of the sternopleural bristle effects of these lines placed them all at approximately 24·7 cM. These mutations are apparently allelic on the basis of a complementation test, and deficiency mapping indicates they occur within chromosomal bands 8A4; 8C6. In situ hybridization analysis of the sites of P element insertions of these lines suggests that mutations probably resulted from excision of P elements at 8C on the original inbred P strain chromosome. Two additional lines, NDC(19) and DP(146), had reduced numbers of sternopleural and abdominal bristles. NDC(19) males had 9·7 fewer abdominal and 8·6 fewer sternopleural bristles than wildtype. The corresponding homozygous abdominal and sternopleural bristle number effects were −5·8 and −3·8, respectively; with the abdominal bristle effect completely recessive and the sternopleural bristle effect nearly additive. DP(146) males had 6·2 fewer abdominal and 4·1 fewer sternopleural bristles than wildtype, with homozygous abdominal bristle effects of −4·3 and sternopleural bristle effects of −2·0. Abdominal bristle effects of this line were partially recessive whereas the sternopleural bristle effects were additive. Physical mapping showed effects on both bristle traits segregated jointly in these two lines, with the NDC(19) mutation closely linked to y and the DP(146) mutation 0·17 cM from it. Complementation tests and deficiency mapping also indicate the mutations in lines NDC(19) and DP(146) are at closely linked but separate loci within chromosomal bands 1B2; 1B4–6 and 1B4–6; 1B10 respectively, with some epistatic effects. In situ hybridization analysis of sites of P element insertion suggest that the NDC(19) mutation, which may be a scute allele, was probably caused by a P element insertion in the IB region; the DP(146) mutation is also associated with an insertion at IB.

scholarly journals Molecular organization and expression of the genetic locus glued in Drosophila melanogaster.

1986 ◽  
Vol 6 (3) ◽  
pp. 833-841 ◽  
Author(s):  
A Swaroop ◽  
J W Sun ◽  
M L Paco-Larson ◽  
A Garen
Keyword(s):  
Drosophila Melanogaster ◽  
Cell Function ◽  
Genetic Locus ◽  
Insertion Site ◽  
Lethal Effect ◽  
P Element ◽  
Molecular Organization ◽  
General Distribution ◽  
Element Insertion ◽  
Mutant Phenotypes

The Glued locus of Drosophila melanogaster is genetically defined as the functional unit which is affected by the dominant Glued mutation Gl. Genomic DNA was cloned from the region of the Glued locus, at 70C2 on chromosome 3, by using a P element insertion in the region as a molecular marker. Three genes encoding polyadenylated transcripts were detected within a 30-kilobase span of the cloned DNA. The gene nearest the P element insertion site was identified as a Glued gene on the basis of alterations in its DNA and encoded transcript associated with the Gl mutation and with reversions of Gl which eliminate the dominant effect by inactivation of the mutant allele. Expression of the wild-type Gl+ gene is temporally regulated during development; the amount of the encoded transcript is highest in the embryonic stage, decreasing in the first and second larval instars, and then increasing in the third instar and pupal stages. There is a maternal contribution of the Gl+ transcript to the embryo, which probably accounts for the maternal lethal effect of Glued mutations on early development. In situ hybridizations of Gl+ DNA to RNA in tissue sections showed that the Gl+ transcript is present in virtually all tissues of the embryo, late larva, and pupa. The general distribution of this transcript is consistent with genetic evidence indicating that the Glued locus controls a generally essential cell function (P. J. Harte and D. R. Kankel, Genetics 101:477-501, 1982). Different Glued mutations produce distinct phenotypic effects, including adults with severe visual defects, larvae lacking imaginal discs, and early lethality. These diverse mutant phenotypes are discussed in terms of quantitative changes in the Glued function. Closely adjacent to Gl+ is another gene which is transcribed in a divergent direction and expressed coordinately with Gl+ throughout Drosophila development. It remains to be determined whether this gene is also involved with the Glued function.

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