Evidence for mobilization of hobo transposons in a P-element mutagenesis screen

Genome ◽  
1993 ◽  
Vol 36 (6) ◽  
pp. 1138-1147 ◽  
Author(s):  
J. Locke ◽  
S. Hanna ◽  
D. Kong
Keyword(s):  
X Chromosome ◽  
Position Effect ◽  
Mobile Element ◽  
P Element ◽  
Position Effect Variegation ◽  
The Third ◽  
Effect Variegation ◽  
Hobo Element ◽  
Transposon Insertions ◽  
P Transposon

In Drosophila melanogaster, mutations in Su(var) and En(var) loci either suppress or enhance position effect variegation, respectively. Towards the cloning of these genes we have induced, recovered, and characterized a series of Su(var) mutations located on the third chromosome. These mutations were recovered from a P-element mutagenesis scheme in which the third chromosome P[ry+ Δ2–3](99B) element would provide transposase in trans to mobilize a single nonautonomous P transposon, P[pUCHSNeo](9C), located on the X chromosome. Although this cross scheme induces mobilization of the X-chromosome P transposons and its subsequent reinsertion onto the autosomes, none of the Su(var) mutations recovered could be associated with P-transposon insertions. Further investigation of these mutations by in situ hybridization showed that another mobile element that can be mobilized in hybrids, hobo, was associated with these mutations. We conclude that the mobilization and reinsertion of the hobo elements, through an inadvertent hybrid HE dysgenic cross, is most likely responsible for the Su(var) mutations recovered from this P-element mutagenesis. The association of hobo elements with this Su(var) locus will facilitate its cloning and offers the possibility of hobo transposon tagging other Su(var) loci.Key words: Drosophila, mobile elements, P element, hobo element, position effect variegation, Su(var).

Enhancer of Polycomb Is a Suppressor of Position-Effect Variegation in Drosophila melanogaster

Genetics ◽  
1998 ◽  
Vol 148 (1) ◽  
pp. 211-220
Author(s):  
Donald A R Sinclair ◽  
Nigel J Clegg ◽  
Jennifer Antonchuk ◽  
Thomas A Milne ◽  
Kryn Stankunas ◽  
...  
Keyword(s):  
Sequence Similarity ◽  
Position Effect ◽  
Polycomb Group ◽  
P Element ◽  
Homeotic Gene ◽  
Position Effect Variegation ◽  
Negative Regulators ◽  
Recombination Mapping ◽  
Effect Variegation ◽  
Homeotic Gene Expression

Abstract Polycomb group (PcG) genes of Drosophila are negative regulators of homeotic gene expression required for maintenance of determination. Sequence similarity between Polycomb and Su(var)205 led to the suggestion that PcG genes and modifiers of position-effect variegation (PEV) might function analogously in the establishment of chromatin structure. If PcG proteins participate directly in the same process that leads to PEV, PcG mutations should suppress PEV. We show that mutations in E(Pc), an unusual member of the PcG, suppress PEV of four variegating rearrangements: In(l)wm4, BSV, T(2;3)SbV, and In(2R)bwVDe2. Using reversion of a P element insertion, deficiency mapping, and recombination mapping as criteria, homeotic effects and suppression of PEV associated with E(Pc) co-map. Asx is an enhancer of PEV, whereas nine other PcG loci do not affect PEV. These results support the conclusion that there are fewer similarities between PcG genes and modifiers of PEV than previously supposed. However, E(Pc) appears to be an important link between the two groups. We discuss why Asx might act as an enhancer of PEV.

scholarly journals Mutation in P0, a Dual Function Ribosomal Protein/Apurinic/Apyrimidinic Endonuclease, Modifies Gene Expression and Position Effect Variegation in Drosophila

Genetics ◽  
1998 ◽  
Vol 150 (4) ◽  
pp. 1487-1495
Author(s):  
Maxim V Frolov ◽  
James A Birchler
Keyword(s):  
Gene Expression ◽  
Ribosomal Protein ◽  
Position Effect ◽  
P Element ◽  
Dual Function ◽  
Insertion Mutant ◽  
Position Effect Variegation ◽  
Element Insertion ◽  
Effect Variegation ◽  
Ribosomal Protein P0

Abstract In a search for modifiers of gene expression with the white eye color gene as a target, a third chromosomal P-element insertion mutant l(3)01544 has been identified that exhibits a strong pigment increase in a white-apricot background. Molecular analysis shows that the P-element insertion is found in the first intron of the gene surrounding the insertion site. Sequencing both the cDNA and genomic fragments revealed that the identified gene is identical to one encoding ribosomal protein P0/apurinic/apyrimidinic endonuclease. The P-element-induced mutation, l(3)01544, affects the steady-state level of white transcripts and transcripts of some other genes. In addition, l(3)01544 suppresses the variegated phenotypes of In(1)wm4h and In(1)y3P, suggesting a potential involvement of the P0 protein in modifying position effect variegation. The revertant generated by the precise excision of the P element has lost all mutant phenotypes. Recent work revealed that Drosophila ribosomal protein P0 contains an apurinic/apyrimidinic endonuclease activity. Our results suggest that this multifunctional protein is also involved in regulation of gene expression in Drosophila.

The heterochromatin-associated protein HP-1 is an essential protein in Drosophila with dosage-dependent effects on position-effect variegation.

Genetics ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 345-352 ◽  
Author(s):  
J C Eissenberg ◽  
G D Morris ◽  
G Reuter ◽  
T Hartnett
Keyword(s):  
Germ Line ◽  
Position Effect ◽  
Inducible Promoter ◽  
Specific Protein ◽  
P Element ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Gene Encoding ◽  
Position Effects ◽  
Effect Variegation

Abstract Chromosome rearrangements which place euchromatic genes adjacent to a heterochromatic breakpoint frequently result in gene repression (position-effect variegation). This repression is thought to reflect the spreading of a heterochromatic structure into neighboring euchromatin. Two allelic dominant suppressors of position-effect variegation were found to contain mutations within the gene encoding the heterochromatin-specific chromosomal protein HP-1. The site of mutation for each allele is given: one converts Lys169 into a nonsense (ochre) codon, while the other is a frameshift after Ser10. In flies heterozygous for one of the mutant alleles (Su(var)2-504), a truncated HP-1 protein was detectable by Western blot analysis. An HP-1 minigene, consisting of HP-1 cDNA under the control of an Hsp70 heat-inducible promoter, was transduced into flies by P element-mediated germ line transformation. Heat-shock driven expression of this minigene results in elevated HP-1 protein level and enhancement of position-effect variegation. Levels of variegating gene expression thus appear to depend upon the level of expression of a heterochromatin-specific protein. The implications of these observations for mechanism of heterochromatic position effects and heterochromatin function are discussed.

scholarly journals The dose of a putative ubiquitin-specific protease affects position-effect variegation in Drosophila melanogaster.

1996 ◽  
Vol 16 (10) ◽  
pp. 5717-5725 ◽  
Author(s):  
S Henchoz ◽  
F De Rubertis ◽  
D Pauli ◽  
P Spierer
Keyword(s):  
Drosophila Melanogaster ◽  
Position Effect ◽  
Transcript Level ◽  
Open Reading Frame ◽  
P Element ◽  
Position Effect Variegation ◽  
Reading Frame ◽  
Effect Variegation ◽  
Specific Protease ◽  
Ubiquitin Specific Protease

A dominant insertional P-element mutation enhances position-effect variegation in Drosophila melanogaster. The mutation is homozygous, viable, and fertile and maps at 64E on the third chromosome. The corresponding gene was cloned by transposon tagging. Insertion of the transposon upstream of the open reading frame correlates with a strong reduction of transcript level. A transgene was constructed with the cDNA and found to have the effect opposite from that of the mutation, namely, to suppress variegation. Sequencing of the cDNA reveals a large open reading frame encoding a putative ubiquitin-specific protease (Ubp). Ubiquitin marks various proteins, frequently for proteasome-dependent degradation. Ubps can cleave the ubiquitin part from these proteins. We discuss the link established here between a deubiquitinating enzyme and epigenetic silencing processes.

Position-effect variegation in Drosophila melanogaster X chromosome inversion with a breakpoint in a satellite block and its suppression in a secondary rearrangement

Chromosoma ◽  
1998 ◽  
Vol 106 (8) ◽  
pp. 520-525 ◽  
Author(s):  
Eugene V. Tolchkov ◽  
Irina A. Kramerova ◽  
Sergei A. Lavrov ◽  
Vanya I. Rasheva ◽  
Silvia Bonaccorsi ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Chromosome Inversion ◽  
Effect Variegation ◽  
Secondary Rearrangement

scholarly journals Dosage-dependent modifiers of position effect variegation in Drosophila and a mass action model that explains their effect.

Genetics ◽  
1988 ◽  
Vol 120 (1) ◽  
pp. 181-198
Author(s):  
J Locke ◽  
M A Kotarski ◽  
K D Tartof
Keyword(s):  
Position Effect ◽  
Class Ii ◽  
Mass Action ◽  
P Element ◽  
Class I ◽  
Gene Copy ◽  
Position Effect Variegation ◽  
Mass Action Model ◽  
Effect Variegation ◽  
Action Model

Abstract Twelve dominant enhancers of position effect variegation, representing four loci on the second and third chromosomes of Drosophila melanogaster, have been induced by P-element mutagenesis. Instead of simple transposon insertions, seven of these mutations are cytologically visible duplications and three are deficiencies. The duplications define two distinct regions, each coinciding with a locus that also behaves as a dominant haplo-dependent suppressor of variegation. Conversely, two of the deficiencies overlap with a region that contains a haplo-dependent enhancer of variegation while duplications of this same region act to suppress variegation. The third deficiency defines another haplo-dependent enhancer. These data indicate that loci capable of modifying variegation do so in an antipodal fashion through changes in the wild-type gene copy number and may be divided into two reciprocally acting classes. Class I modifiers enhance variegation when duplicated or suppress variegation when deficient. Class II modifiers enhance when deficient but suppress when duplicated. From our data, and those of others, we propose that in Drosophila there are about 20 to 30 dominant loci that modify variegation. Most appear to be of the class I type whereas only two class II modifiers have been identified so far. From these observations we put forth a model, based on the law of mass action, for understanding how such suppressor-enhancer loci function. We propose that each class I modifier codes for a structural protein component of heterochromatin and their effects on variegation are a consequence of their dosage dependent influence on the extent of the assembly of heterochromatin at the chromosomal site of the position effect. It is further proposed that class II modifiers may inhibit the class I products directly, bind to hypothetical termination sites that define heterochromatin boundaries or promote euchromatin formation. Consistent with our mass action model we find that combining two enhancers together produce additive and not epistatic effects. Also, since different enhancers have different relative strengths on different variegating mutants, we suggest that heterochromatic domains are constructed by a combinatorial association of proteins. The mass action model proposed here is of general significance for any assembly driven reaction and has implications for understanding a wide variety of biological phenomena.(ABSTRACT TRUNCATED AT 400 WORDS)

Position-effect variegation in Drosophila depends on dose of the gene encoding the E2F transcriptional activator and cell cycle regulator

Development ◽  
1996 ◽  
Vol 122 (6) ◽  
pp. 1949-1956 ◽  
Author(s):  
C. Seum ◽  
A. Spierer ◽  
D. Pauli ◽  
J. Szidonya ◽  
G. Reuter ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Opposite Effect ◽  
Null Allele ◽  
Position Effect ◽  
Transcriptional Activator ◽  
P Element ◽  
Position Effect Variegation ◽  
Gene Encoding ◽  
Cell Cycle Regulator ◽  
Effect Variegation

A dominant mutation due to the insertion of a P-element at 93E on the third chromosome of Drosophila melanogaster enhances position-effect variegation. The corresponding gene was cloned by transposon tagging and the sequence of the transcript revealed that it corresponds to the gene encoding the transcriptional activator and cell cycle regulator dE2F. The transposon-tagged allele is homozygous viable, and the insertion of the transposon in an intron correlates with a strong reduction in the amount of transcript. A homozygous lethal null allele was found to behave as a strong enhancer when heterozygous. Overexpression of the gene in transgenic flies has the opposite effect of suppressing variegation. A link is established here, and discussed, between the dose of a transcriptional activator, which controls the cell cycle, and epigenetic silencing of chromosomal domains in Drosophila.

scholarly journals Genomic Imprinting and Position-Effect Variegation in Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1503-1516 ◽  
Author(s):  
Vett K Lloyd ◽  
Don A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Imprinting ◽  
X Chromosome ◽  
Position Effect ◽  
Specific Effect ◽  
Position Effect Variegation ◽  
Mitotic Instability ◽  
Effect Variegation ◽  
Allele Specific ◽  
The Individual

Abstract Genomic imprinting is a phenomenon in which the expression of a gene or chromosomal region depends on the sex of the individual transmitting it. The term imprinting was first coined to describe parent-specific chromosome behavior in the dipteran insect Sciara and has since been described in many organisms, including other insects, plants, fish, and mammals. In this article we describe a mini-X chromosome in Drosophila melanogaster that shows genomic imprinting of at least three closely linked genes. The imprinting of these genes is observed as mosaic silencing when the genes are transmitted by the male parent, in contrast to essentially wild-type expression when the same genes are maternally transmitted. We show that the imprint is due to the sex of the parent rather than to a conventional maternal effect, differential mitotic instability of the mini-X chromosome, or an allele-specific effect. Finally, we have examined the effects of classical modifiers of position-effect variegation on the maintenance and the establishment of the imprint. Factors that modify position-effect variegation alter the somatic expression but not the establishment of the imprint. This suggests that chromatin structure is important in maintenance of the imprint, but a separate mechanism may be responsible for its initiation.

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