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.

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 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.

scholarly journals The AT-Hook Protein D1 Is Essential for Drosophila melanogaster Development and Is Implicated in Position-Effect Variegation

2002 ◽  
Vol 22 (4) ◽  
pp. 1218-1232 ◽  
Author(s):  
Nathalie Aulner ◽  
Caroline Monod ◽  
Guillaume Mandicourt ◽  
Denis Jullien ◽  
Olivier Cuvier ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Position Effect ◽  
D1 Protein ◽  
P Element ◽  
Centromeric Heterochromatin ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Mrna Levels ◽  
Satellite Repeats ◽  
Effect Variegation

ABSTRACT We have analyzed the expression pattern of the D1 gene and the localization of its product, the AT hook-bearing nonhistone chromosomal protein D1, during Drosophila melanogaster development. D1 mRNAs and protein are maternally contributed, and the protein localizes to discrete foci on the chromosomes of early embryos. These foci correspond to 1.672- and 1.688-g/cm3 AT-rich satellite repeats found in the centromeric heterochromatin of the X and Y chromosomes and on chromosomes 3 and 4. D1 mRNA levels subsequently decrease throughout later development, followed by the accumulation of the D1 protein in adult gonads, where two distributions of D1 can be correlated to different states of gene activity. We show that the EP473 mutation, a P-element insertion upstream of D1 coding sequences, affects the expression of the D1 gene and results in an embryonic homozygous lethal phenotype correlated with the depletion of D1 protein during embryogenesis. Remarkably, decreased levels of D1 mRNA and protein in heterozygous flies lead to the suppression of position-effect variegation (PEV) of the white gene in the white-mottled (wm4h ) X-chromosome inversion. Our results identify D1 as a DNA-binding protein of known sequence specificity implicated in PEV. D1 is the primary factor that binds the centromeric 1.688-g/cm3 satellite repeats which are likely involved in white-mottled variegation. We propose that the AT-hook D1 protein nucleates heterochromatin assembly by recruiting specialized transcriptional repressors and/or proteins involved in chromosome condensation.

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 Position effect variegation in Drosophila melanogaster: relationship between suppression effect and the amount of Y chromosome.

Genetics ◽  
1989 ◽  
Vol 122 (4) ◽  
pp. 793-800 ◽  
Author(s):  
P Dimitri ◽  
C Pisano
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Position Effect ◽  
Chromosome Rearrangements ◽  
Position Effect Variegation ◽  
Position Effects ◽  
Suppression Effect ◽  
Genetic Nature ◽  
Cell Clones ◽  
Effect Variegation

Abstract Position effect variegation results from chromosome rearrangements which translocate euchromatic genes close to the heterochromatin. The euchromatin-heterochromatin association is responsible for the inactivation of these genes in some cell clones. In Drosophila melanogaster the Y chromosome, which is entirely heterochromatic, is known to suppress variegation of euchromatic genes. In the present work we have investigated the genetic nature of the variegation suppressing property of the D. melanogaster Y chromosome. We have determined the extent to which different cytologically characterized Y chromosome deficiencies and Y fragments suppress three V-type position effects: the Y-suppressed lethality, the white mottled and the brown dominant variegated phenotypes. We find that: (1) chromosomes which are cytologically different and yet retain similar amounts of heterochromatin are equally effective suppressors, and (2) suppression effect is positively related to the size of the Y chromosome deficiencies and fragments that we tested. It increases with increasing amounts of Y heterochromatin up to 60-80% of the entire Y, after which the effect reaches a plateau. These findings suggest suppression is a function of the amount of Y heterochromatin present in the genome and is not attributable to any discrete Y region.

scholarly journals Mutations of zeste that mediate transvection are recessive enhancers of position-effect variegation in Drosophila melanogaster.

Genetics ◽  
1995 ◽  
Vol 141 (1) ◽  
pp. 245-253 ◽  
Author(s):  
B H Judd
Keyword(s):  
Transcription Factor ◽  
Drosophila Melanogaster ◽  
Transposable Elements ◽  
Chromosomal Rearrangement ◽  
Position Effect ◽  
Dna Binding Protein ◽  
Position Effect Variegation ◽  
Effect Variegation ◽  
Null State

Abstract Evidence is presented demonstrating that mutations of zeste, particularly the null state, are strong recessive enhancers of position-effect variegation (PEV) for the white, roughest and Notch loci. The zeste locus encodes a DNA-binding protein that acts as a transcription factor and mediates transvection phenomena at several loci. Its involvement with these seemingly diverse phenomena suggests that the normal zeste product functions in the decondensation of chromatin. A model is presented proposing that zeste is important for opening and stabilizing domains of chromatin, a step in gene determination and the establishment of cell memory. It postulates that chromatin domains that have been structurally modified by chromosomal rearrangement or by insertion of transposable elements are particularly sensitive to the absence or modification of the zeste protein. Such a view unifies the role of zeste in transcription, transvection and PEV.

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.

scholarly journals HISTONE GENE MULTIPLICITY AND POSITION EFFECT VARIEGATION IN DROSOPHILA MELANOGASTER

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 327-344
Author(s):  
Gerald D Moore ◽  
Donald A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Chromosome ◽  
Current Knowledge ◽  
Position Effect ◽  
Histone Gene ◽  
Position Effect Variegation ◽  
Chromosome 2 ◽  
Gene Complex ◽  
Position Effects ◽  
Effect Variegation

ABSTRACT The histone genes of wild-type Drosophila melanogaster are reiterated 100–150 times per haploid genome and are located in the segment of chromosome 2 that corresponds to polytene bands 39D2-3 to E1-2. The influence of altered histone gene multiplicity on chromatin structure has been assayed by measuring modification of the gene inactivation associated with position effect variegation in genotypes bearing deletions of the 39D-E segment. The proportion of cells in which a variegating gene is active is increased in genotypes that are heterozygous for a deficiency that removes the histone gene complex. Deletions that remove segments adjacent to the histone gene complex have no effect on the expression of variegating genes. Suppression of position effect variegation associated with reduction of histone gene multiplicity applies to both X-linked and autosomal variegating genes. Position effects exerted by both autosomal and sex-chromosome heterochromatin were suppressible by deletions of the histone gene complex. The suppression was independent of the presence of the Y chromosome. A deficiency that deletes only the distal portion of the histone gene complex also has the ability to suppress position effect variegation. Duplication of the histone gene complex did not enhance position effect variegation. Deletion or duplication of the histone gene complex in the maternal genome had no effect on the extent of variegation in progeny whose histone gene multiplicity was normal. These results are discussed with respect to current knowledge of the organization of the histone gene complex and control of its expression.

scholarly journals The effect of modifiers of position-effect variegation on the variegation of heterochromatic genes of Drosophila melanogaster.

Genetics ◽  
1991 ◽  
Vol 128 (4) ◽  
pp. 785-797 ◽  
Author(s):  
M G Hearn ◽  
A Hedrick ◽  
T A Grigliatti ◽  
B T Wakimoto
Keyword(s):  
Drosophila Melanogaster ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Chromosome 2 ◽  
Wild Type ◽  
Regulatory Requirements ◽  
Expression Of Genes ◽  
Effect Variegation ◽  
Type Gene ◽  
Heterochromatic Genes

Abstract Dominant modifiers of position-effect variegation of Drosophila melanogaster were tested for their effects on the variegation of genes normally located in heterochromatin. These modifiers were previously isolated as strong suppressors of the variegation of euchromatic genes and have been postulated to encode structural components of heterochromatin or other products that influence chromosome condensation. While eight of the modifiers had weak or no detectable effects, six acted as enhancers of light (lt) variegation. The two modifiers with the strongest effects on lt were shown to also enhance the variegation of neighboring heterochromatic genes. These results suggest that the wild-type gene products of some modifiers of position-effect variegation are required for proper expression of genes normally located within or near the heterochromatin of chromosome 2. We conclude that these heterochromatic genes have fundamentally different regulatory requirements compared to those typical of euchromatic genes.

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