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.

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 Interactions Among Dosage-Dependent Trans-Acting Modifiers of Gene Expression and Position-Effect Variegation in Drosophila

Genetics ◽  
1998 ◽  
Vol 150 (1) ◽  
pp. 251-263 ◽  
Author(s):  
Utpal Bhadra ◽  
Manika Pal Bhadra ◽  
James A Birchler
Keyword(s):  
Gene Expression ◽  
Quantitative Traits ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Developmental Transitions ◽  
Eye Color ◽  
Dosage Effects ◽  
Effect Variegation ◽  
Hierarchical Manner ◽  
Color Gene

Abstract We have investigated the effect of dosage-dependent trans-acting regulators of the white eye color gene in combinations to understand their interaction properties. The consequences of the interactions will aid in an understanding of aneuploid syndromes, position-effect variegation (PEV), quantitative traits, and dosage compensation, all of which are affected by dosage-dependent modifiers. Various combinations modulate two functionally related transcripts, white and scarlet, differently. The overall trend is that multiple modifiers are noncumulative or epistatic to each other. In some combinations, developmental transitions from larvae to pupae to adults act as a switch for whether the effect is positive or negative. With position-effect variegation, similar responses were found as with gene expression. The highly multigenic nature of dosage-sensitive modulation of both gene expression and PEV suggests that dosage effects can be progressively transduced through a series of steps in a hierarchical manner.

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.

Evidence for intrinsic differences in the formation of chromatin domains in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 132 (4) ◽  
pp. 1063-1069 ◽  
Author(s):  
C P Bishop
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Genetic Background ◽  
Position Effect ◽  
The Other ◽  
Position Effect Variegation ◽  
Compaction Process ◽  
Chromatin Domains ◽  
Effect Variegation ◽  
Reporter Systems

Abstract The results of an investigation into intrinsic differences in the formation of two different heterochromatic domains are presented. The study utilized two different position effect variegation mutants in Drosophila melanogaster for investigating the process of compacting different stretches of DNA into heterochromatin. Each stretch of DNA encodes for a gene that affects different aspects of bristle morphology. The expression of each gene is prevented when it is compacted into heterochromatin thus the genes serve as effective reporter systems to monitor the spread of heterochromatin. Both variegating mutants are scored in the same cell such that environmental and genetic background differences are unambiguously eliminated. Any differences observed in the repression of the two genes must therefore be the result of intrinsic differences in the heterochromatic compaction process for the two stretches of DNA. Studies of the effects different enhancers of variegation have upon the compaction of the two genes indicate each compaction event occurs independently of the other, and that different components are involved in the two processes. These results are discussed with regard to spreading heterochromatin and the role this process may play in regulating gene expression.

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.

Genetic factors controlling white gene expression of the transposon AR4-24 at a telomere in Drosophila melanogaster

Genome ◽  
2002 ◽  
Vol 45 (6) ◽  
pp. 1025-1034 ◽  
Author(s):  
M L Balasov
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Genetic Factors ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Heterochromatin Protein 1 ◽  
Heterochromatin Protein ◽  
Effect Variegation ◽  
Restricted Pattern

The position effect of the AR 4-24 P[white, rosy] transposon was studied at cytological position 60F. Three copies of the transposon (within ~50-kb region) resulted in a spatially restricted pattern of white variegation. This pattern was modified by temperature and by removal of the Y chromosome, suggesting that it was due to classical heterochromatin-induced position effect variegation (PEV). In contrast with classical PEV, extra dose of the heterochromatin protein 1 (HP1) suppressed white variegation and one dose enhanced it. The effect of Pc-G, trx-G, and other PEV suppressors was also tested. It was found that E(Pc)1, TrlR85, and mutations of Su(z)2C relieve AR 4-24- silencing and z1 enhances it. To explain the results obtained with these modifiers, it is proposed that PEV and telomeric position effect can counteract each other at this particular cytological site.Key words: position effect variegation, heterochromatin protein 1, Drosophila melanogaster.

scholarly journals Weakener of white (Wow), a gene that modifies the expression of the white eye color locus and that suppresses position effect variegation in Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 137 (4) ◽  
pp. 1057-1070 ◽  
Author(s):  
J A Birchler ◽  
U Bhadra ◽  
L Rabinow ◽  
R Linsk ◽  
A T Nguyen-Huynh
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Position Effect ◽  
Northern Analysis ◽  
Regulatory Sequences ◽  
Position Effect Variegation ◽  
Eye Color ◽  
Effect Variegation ◽  
Modifying Effect ◽  
Color Gene

Abstract A locus is described in Drosophila melanogaster that modifies the expression of the white eye color gene. This trans-acting modifier reduces the expression of the white gene in the eye, but elevates the expression in other adult tissues. Because of the eye phenotype in which the expression of white is lessened but not eliminated, the newly described locus is called the Weakener of white (Wow). Northern analysis reveals that Wow can exert an inverse or direct modifying effect depending upon the developmental stage. Two related genes, brown and scarlet, that are coordinately expressed with white, are also affected by Wow. In addition, Wow modulates the steady state RNA level of the retrotransposon, copia. When tested with a white promoter-Alcohol dehydrogenase reporter. Wow confers the modifying effect to the reporter, suggesting a requirement of the white regulatory sequences for mediating the response. In addition to being a dosage sensitive regulator of white, brown, scarlet and copia, Wow acts as a suppressor of position effect variegation. There are many dosage sensitive suppressors of position effect variegation and many dosage-sensitive modifiers of gene expression. The Wow mutations provide evidence for an overlap between the two types of modifiers.

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.

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