scholarly journals The genomic silencing of position-effect variegation in Drosophila melanogaster: interaction between the heterochromatin-associated proteins Su(var)3-7 and HP1

2000 ◽  
Vol 113 (23) ◽  
pp. 4253-4261 ◽  
Author(s):  
M. Delattre ◽  
A. Spierer ◽  
C.H. Tonka ◽  
P. Spierer
Keyword(s):  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Pericentric Heterochromatin ◽  
Position Effect Variegation ◽  
Effect Variegation ◽  
Associated Proteins ◽  
Chromo Shadow Domain ◽  
Two Hybrid ◽  
Hp1 Proteins

Position-effect variegation results from mosaic silencing by chromosomal rearrangements juxtaposing euchromatin genes next to pericentric heterochromatin. An increase in the amounts of the heterochromatin-associated Su(var)3-7 and HP1 proteins augments silencing. Using the yeast two-hybrid protein interaction trap system, we have isolated HP1 using Su(var)3-7 as a bait. We have then delimited three binding sites on Su(var)3-7 for HP1. On HP1, the C-terminal moiety, including the chromo shadow domain, is required for interaction. In vivo, both proteins co-localise not only in heterochromatin, but also in a limited set of sites in euchromatin and at telomeres. When delocalised to the sites bound by the protein Polycomb in euchromatin, HP1 recruits Su(var)3-7. Finally, and in contrast with euchromatin genes, a decrease in the amounts of both proteins enhances variegation of the light gene, one of the few genetic loci mapped within pericentric heterochromatin. This body of data supports a direct link between Su(var)3-7 and HP1 in the genomic silencing of position-effect variegation.

scholarly journals Cis-effects of heterochromatin on heterochromatic and euchromatic gene activity in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 140 (3) ◽  
pp. 1033-1045
Author(s):  
M Howe ◽  
P Dimitri ◽  
M Berloco ◽  
B T Wakimoto
Keyword(s):  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Regulatory Requirements ◽  
Molecular Studies ◽  
Effect Variegation ◽  
Novel Method ◽  
In Cis ◽  
Derivatives Of ◽  
Heterochromatic Genes

Abstract Chromosomal rearrangements that juxtapose heterochromatin and euchromatin can result in mosaic inactivation of heterochromatic and euchromatic genes. This phenomenon, position effect variegation (PEV), suggests that heterochromatic and euchromatic genes differ in their regulatory requirements. This report describes a novel method for mapping regions required for heterochromatic genes, and those that induce PEV of a euchromatic gene. P transposase mutagenesis was used to generate derivatives of a translocation that variegated for the light+ (lt+) gene and carried the euchromatic white+ (w+) gene on a transposon near the heterochromatin-euchromatin junction. Cytogenetic and genetic analyses of the derivatives showed that P mutagenesis resulted in deletions of several megabases of heterochromatin. Genetic and molecular studies showed that the derivatives shared a euchromatic breakpoint but differed in their heterochromatic breakpoint and their effects on seven heterochromatic genes and the w+ gene. Heterochromatic genes differed in their response to deletions. The lt+ gene was sensitive to the amount of heterochromatin at the breakpoint but the heterochromatic 40Fa gene was not. The severity of variegated w+ phenotype did not depend on the amount of heterochromatin in cis, but varied with local heterochromatic environment. These data are relevant for considering mechanisms of PEV of both heterochromatic and euchromatic genes.

Suppressors of position-effect variegation in Drosophila melanogaster affect expression of the heterochromatic gene light in the absence of a chromosome rearrangement

Genome ◽  
1998 ◽  
Vol 41 (4) ◽  
pp. 495-503 ◽  
Author(s):  
N J Clegg ◽  
B M Honda ◽  
I P Whitehead ◽  
T A Grigliatti ◽  
B Wakimoto ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Centromeric Heterochromatin ◽  
Position Effect Variegation ◽  
Gene Products ◽  
Affect Expression ◽  
Effect Variegation ◽  
Heterochromatic Genes ◽  
Var Gene

Suppressors of position-effect variegation (Su(var)s) in Drosophila melanogaster are usually studied in the presence of chromosomal rearrangements, which exhibit variegated expression of euchromatic genes moved near to, or heterochromatic genes moved away from, centromeric heterochromatin. However, the effects of Su(var) mutations on heterochromatic gene expression in the absence of a variegating re-arrangement have not yet been defined. Here we present a number of results which suggest that Su(var) gene products can interact to affect the expression of the light gene in its normal heterochromatic location. We initially observed that eye pigment was reduced in several Su(var) double mutants; the phenotype resembled that of light mutations and was more severe when only one copy of the light gene was present. This reduced pigmentation could be alleviated by a duplication for the light gene or by a reduction in the amount of cellular heterochromatin. In addition, the viability of most Su(var) double mutant combinations tested was greatly reduced in a genetic background of reduced light gene dosage, when extra heterochromatin is present. We conclude that Su(var) gene products can affect expression of the heterochromatic light gene in the absence of any chromosomal rearrangements. However, it is noteworthy that mutations in any single Su(var) gene have little effect on light expression; we observe instead that different pairings of Su(var) mutations are required to show an effect on light expression. Interestingly, we have obtained evidence that at least two of the second chromosome Su(var) mutations are gain-of-function lesions, which also suggests that there may be different modes of interaction among these genes. It may therefore be possible to use this more sensitive assay of Su(var) effects on heterochromatic genes to infer functional relationships among the products of the 50 or more known Su(var) loci.Key words: heterochromatin, chromatin, gene interactions.

scholarly journals The role of heterochromatin in the expression of a heterochromatic gene, the rolled locus of Drosophila melanogaster.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 277-292 ◽  
Author(s):  
D F Eberl ◽  
B J Duyf ◽  
A J Hilliker
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Centromeric Heterochromatin ◽  
Position Effect Variegation ◽  
Position Effects ◽  
Major Function ◽  
Effect Variegation ◽  
Heterochromatic Genes

Abstract Constitutive heterochromatic regions of chromosomes are those that remain condensed through most or all of the cell cycle. In Drosophila melanogaster, the constitutive heterochromatic regions, located around the centromere, contain a number of gene loci, but at a much lower density than euchromatin. In the autosomal heterochromatin, the gene loci appear to be unique sequence genes interspersed among blocks of highly repeated sequences. Euchromatic genes do not function well when brought into the vicinity of heterochromatin (position-effect variegation). We test the possibility that the blocks of centromeric heterochromatin provide an environment essential for heterochromatic gene function. To assay directly the functional requirement of autosomal heterochromatic genes to reside in heterochromatin, the rolled (rl) gene, which is normally located deep in chromosome 2R heterochromatin, was relocated within small blocks of heterochromatin to a variety of euchromatic positions by successive series of chromosomal rearrangements. The function of the rl gene is severely affected in rearrangements in which the rl gene is isolated in a small block of heterochromatin, and these position effects can be reverted by rearrangements which bring the rl gene closer to any large block of autosomal or X chromosome heterochromatin. There is some evidence that five other 2R heterochromatic genes are also affected among these rearrangements. These findings demonstrate that the heterochromatic genes, in contrast to euchromatic genes whose function is inhibited by relocation to heterochromatin, require proximity to heterochromatin to function properly, and they argue strongly that a major function of the highly repeated satellite DNA, which comprises most of the heterochromatin, is to provide this heterochromatic environment.

Functional dissection of theDrosophilamodifier of variegationSu(var)3-7

Development ◽  
2002 ◽  
Vol 129 (17) ◽  
pp. 3975-3982 ◽  
Author(s):  
Yannis Jaquet ◽  
Marion Delattre ◽  
Anne Spierer ◽  
Pierre Spierer
Keyword(s):  
Specific Binding ◽  
Zinc Fingers ◽  
Position Effect ◽  
Pericentric Heterochromatin ◽  
Dominant Negative ◽  
Dominant Negative Effect ◽  
Position Effect Variegation ◽  
N Terminus ◽  
Effect Variegation ◽  
Negative Effect

An increase in the dose of the heterochromatin-associated Su(var)3-7 protein of Drosophila augments the genomic silencing of position-effect variegation. We have expressed a number of fragments of the protein in flies to assign functions to the different domains. Specific binding to pericentric heterochromatin depends on the C-terminal half of the protein. The N terminus, containing six of the seven widely spaced zinc fingers, is required for binding to bands on euchromatic arms, with no preference for pericentric heterochromatin. In contrast to the enhancing properties of the full-length protein, the N terminus half has no effect on heterochromatin-dependent position-effect variegation. In contrast, the C terminus moiety suppresses variegation. This dominant negative effect on variegation could result from association of the fragment with the wild type endogenous protein. Indeed, we have found and mapped a domain of self-association in this C-terminal half. Furthermore, a small fragment of the C-terminal region actually depletes pericentric heterochromatin from endogenous Su(var)3-7 and has a very strong suppressor effect. This depletion is not followed by a depletion of HP1, a companion of Su(var)3-7. This indicates that Su(var)3-7 does not recruit HP1 to heterochromatin. We propose in conclusion that the association of Su(var)3-7 to heterochromatin depends on protein-protein interaction mediated by the C-terminal half of the sequence, while the silencing function requires also the N-terminal half containing the zinc fingers.

scholarly journals Comparative Analysis of Position–Effect Variegation Mutations in Drosophila melanogaster Delineates the Targets of Modifiers

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 733-741
Author(s):  
Georgette L Sass ◽  
Steven Henikoff
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Reporter Genes ◽  
Class Ii ◽  
Class I ◽  
Position Effect Variegation ◽  
Heterochromatin Formation ◽  
Transposon Insertion ◽  
Effect Variegation

Abstract In Drosophila melanogaster, heterochromatin-induced silencing or position–effect variegation (PEV) of a reporter gene has provided insights into the properties of heterochromatin. Class I modifiers suppress PEV, and class II modifiers enhance PEV when the modifier gene is present in fewer than two doses. We have examined the effects of both class I and class II modifiers on four PEV mutations. These mutations include the inversions In(1)wm4 and In(2R)bwVDe2, which are classical chromosomal rearrangements that typify PEV mutations. The other mutations are a derivative of brownDominant, in which brown+ reporters are inactivated by a large block of heterochromatin, and a P[white+] transposon insertion associated with second chromosome heterochromatin. In general, we find that class I modifiers affect both classical and nonclassical PEV mutations, whereas class II modifiers affect only classical PEV mutations. We suggest that class II modifiers affect chromatin architecture in the vicinity of reporter genes, and only class I modifiers identify proteins that are potentially involved in heterochromatin formation or maintenance. In addition, our observations support a model in which there are different constraints on the process of heterochromatin-induced silencing in classical vs. nonclassical PEV mutations.

scholarly journals Microwave influence on the position effect variegation in Drosophila melanogaster Meig.

2018 ◽  
Vol 23 ◽  
pp. 363-368
Author(s):  
L. D. Dyka ◽  
V. Yu. Strashnyuk
Keyword(s):  
Drosophila Melanogaster ◽  
Microwave Irradiation ◽  
Gene Silencing ◽  
Power Density ◽  
Position Effect ◽  
Pericentric Heterochromatin ◽  
Position Effect Variegation ◽  
Irradiation Intensity ◽  
Genetic Inactivation ◽  
Effect Variegation

Aim. The purpose of investigation was to study the effect of microwave irradiation of different intensity on the manifestation of the position effect variegation (PEV) in Drosophila melanogaster Meig. Methods. Experiments were carried out on mutant strain In(1)wm4, y. Microwave radiation with frequency 36.64 GHz and power density 0.01; 0.1 and 1 W/m2, was used. Exposure to microwaves was applied in early embryogenesis after 2-hour oviposition. Exposure time was 30 sec. PEV was examined in the irradiated and non-irradiated (control) flies. Results. In females, microwave irradiation at a power density of 1 W/m2 led to an enhance in the inactivation of the white+ gene transferred into a vicinity of pericentric heterochromatin in the X-chromosome. No effect was detected by irradiation intensity of 0.01 and 0.1 W/m2. In males, there was a suppression of genetic inactivation at a power density of 0.01 W/m2. Conclusions. Microwave irradiation can affect the size of heterochromatin blocks that cause gene silencing in PEV. The effect depends on the sex and intensity of the radiation. Keywords: Drosophila melanogaster Meig., position effect variegation, heterochromatin, gene silencing, non-ionising radiation.

scholarly journals A Reexamination of Spreading of Position-Effect Variegation in the white-roughest Region of Drosophila melanogaster

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 259-272 ◽  
Author(s):  
Paul B Talbert ◽  
Steven Henikoff
Keyword(s):  
Chromosomal Rearrangements ◽  
Position Effect ◽  
White Gene ◽  
Position Effect Variegation ◽  
Continuous Linear ◽  
Effect Variegation ◽  
Drosophila Heterochromatin ◽  
In Trans ◽  
Linear Propagation ◽  
Rearrangement Breakpoint

Abstract In Drosophila, heterochromatin causes mosaic silencing of euchromatic genes brought next to it by chromosomal rearrangements. Silencing has been observed to “spread”: genes closer to the heterochromatic rearrangement breakpoint are silenced more frequently than genes farther away. We have examined silencing of the white and roughest genes in the variegating rearrangements In(1)wm4, In(1)wmMc, and In(1)wm51b. Eleven stocks bearing these chromosomes differ widely in the strength of silencing of white and roughest. Stock-specific differences in the relative frequencies of inactivation of white and roughest were found that map to the white-roughest region or the adjacent heterochromatin. Most stock-specific differences did not correlate with gross differences in the heterochromatic content of the rearranged chromosomes; however, two stocks, In(1)wm51b and In(1)wmMc, were found to have anomalous additional heterochromatin that may act in trans to suppress variegating alleles. In comparing different stocks, the frequency of silencing of the roughest gene, which is more distant from heterochromatin, does not correlate with the frequency of silencing of the more proximal white gene on the same chromosome, in contradiction to the expectation of models of continuous linear propagation of silencing. We frequently observed rough eye tissue that is pigmented, as though an active white gene is skipped.

scholarly journals CYTOGENETIC LOCALIZATION OF THE ACID PHOSPHATASE-1 GENE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1978 ◽  
Vol 88 (3) ◽  
pp. 487-497
Author(s):  
William J Morrison ◽  
Ross J MacIntyre
Keyword(s):  
Drosophila Melanogaster ◽  
Acid Phosphatase ◽  
Y Chromosome ◽  
Chromosomal Rearrangements ◽  
Position Effect ◽  
Chromosome 3 ◽  
Position Effect Variegation ◽  
Effect Variegation

ABSTRACT A translocation in which a segment of chromosome 3 is inserted into the Y chromosome was found to contain the acid phosphatase-1 gene (Acph-1). In flies hyperploid for that gene, acid phosphatase-1 levels are proportional to the dose of the gene. The locus is placed within the salivary chromosome subdivisions 99D and 99E on the basis of its inclusion in the translocated segment and on the previous placement of the claret locus. Several chromosomal rearrangements involving heterochromatic breakpoints and euchromatic breakpoints adjacent to 99D-99E were tested for possible position-effect variegation of acid phosphatase-1. No decrease in the synthesis of the electrophoretic subunit encoded by the relocated gene was observed within any of the rearrangements.

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