scholarly journals A lot about a little dot — lessons learned from Drosophila melanogaster chromosome 4This paper is one of a selection of papers published in this Special Issue, entitled 29th Annual International Asilomar Chromatin and Chromosomes Conference, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 87 (1) ◽  
pp. 229-241 ◽  
Author(s):  
Nicole C. Riddle ◽  
Christopher D. Shaffer ◽  
Sarah C.R. Elgin
Keyword(s):  
Drosophila Melanogaster ◽  
Peer Review Process ◽  
Position Effect ◽  
Polytene Chromosomes ◽  
Lessons Learned ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Chromosome 4 ◽  
Fourth Chromosome ◽  
Heterochromatin Protein 1

The fourth chromosome of Drosophila melanogaster has a number of unique properties that make it a convenient model for the study of chromatin structure. Only 4.2 Mb overall, the 1.2 Mb distal arm of chromosome 4 seen in polytene chromosomes combines characteristics of heterochromatin and euchromatin. This domain has a repeat density of ~35%, comparable to some pericentric chromosome regions, while maintaining a gene density similar to that of the other euchromatic chromosome arms. Studies of position-effect variegation have revealed that heterochromatic and euchromatic domains are interspersed on chromosome 4, and both cytological and biochemical studies have demonstrated that chromosome 4 is associated with heterochromatic marks, such as heterochromatin protein 1 and histone 3 lysine 9 methylation. Chromosome 4 is also marked by POF (painting-of-fourth), a chromosome 4-specific chromosomal protein, and utilizes a dedicated histone methyltransferase, EGG. Studies of chromosome 4 have helped to shape our understanding of heterochromatin domains and their establishment and maintenance. In this review, we provide a synthesis of the work to date and an outlook to the future.

scholarly journals A heat-shock-activated cDNA encoding GAGA factor rescues some lethal mutations in the Drosophila melanogaster Trithorax-like gene

2001 ◽  
Vol 78 (1) ◽  
pp. 13-21 ◽  
Author(s):  
H. GRANOK ◽  
B. A. LEIBOVITCH ◽  
S. C. R. ELGIN
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Position Effect ◽  
Efficient Production ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Gaga Factor ◽  
Genetic Rescue ◽  
Regulation Of Synthesis

GAGA factor is an important chromosomal protein involved in establishing specific nucleosome arrays and in regulating gene transcription in Drosophila melanogaster. We developed a transgenic system for controlled heat-shock-dependent overexpression of the GAGA factor 519 amino acid isoform (GAGA-519) in vivo. Efficient production of stable protein from these transgenes provided genetic rescue of a hypomorphic Trithorax-like (Trl) lethal allele to adulthood. Nevertheless, supplemental GAGA-519 did not suppress position effect variegation (PEV), a phenomenon commonly used to measure dosage effects of chromosomal proteins, nor did it rescue other lethal alleles of Trl. The results suggest requirements for the additional isoforms of GAGA factor, or for more precise regulation of synthesis, to carry out the diverse functions of this protein.

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 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.

Effect of the Suppressor of Underreplication (SuUR) Gene on Position-Effect Variegation Silencing in Drosophila melanogaster

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1209-1220
Author(s):  
E S Belyaeva ◽  
L V Boldyreva ◽  
E I Volkova ◽  
R A Nanayev ◽  
A A Alekseyenko ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Position Effect ◽  
Polytene Chromosomes ◽  
Morphological Characters ◽  
Position Effect Variegation ◽  
Dependent Manner ◽  
Dose Dependent ◽  
Suur Protein ◽  
Chromosome Regions ◽  
Suur Gene

Abstract It has been previously shown that the SuUR gene encodes a protein located in intercalary and pericentromeric heterochromatin in Drosophila melanogaster polytene chromosomes. The SuUR mutation suppresses the formation of ectopic contacts and DNA underreplication in polytene chromosomes; SuUR+ in extra doses enhances the expression of these characters. This study demonstrates that heterochromatin-dependent PEV silencing is also influenced by SuUR. The SuUR protein localizes to chromosome regions compacted as a result of PEV; the SuUR mutation suppresses DNA underreplication arising in regions of polytene chromosomes undergoing PEV. The SuUR mutation also suppresses variegation of both adult morphological characters and chromatin compaction observed in rearranged chromosomes. In contrast, SuUR+ in extra doses and its overexpression enhance variegation. Thus, SuUR affects PEV silencing in a dose-dependent manner. However, its effect is expressed weaker than that of the strong modifier Su(var)2-5.

Varied expression of a Y-linked P[w+] insert due to imprinting in Drosophila melanogaster

Genome ◽  
2000 ◽  
Vol 43 (2) ◽  
pp. 285-292 ◽  
Author(s):  
Bethany S Haller ◽  
R C Woodruff
Keyword(s):  
Drosophila Melanogaster ◽  
Y Chromosome ◽  
Genetic Background ◽  
Position Effect ◽  
P Element ◽  
Parental Origin ◽  
Position Effect Variegation ◽  
Reporter System ◽  
Heterochromatin Protein 1 ◽  
Parental Female

During gametogenesis, a gene can become imprinted affecting its expression in progeny. We have used the expression of a Y-linked P[w+]YAL transposable DNA element as a reporter system to investigate the effect of parental origination on the expression of the w+ insert. Expression of w+ was greater in male progeny when the Y chromosome, harboring the insert, was inherited from the parental male rather than from the parental female. Imprinting was not due to a genetic background influence in the males, since the only difference among the males was the parental origin of the Y chromosome. It was also observed that the genetic background can affect imprinting, since w+ expression was also higher in males when the Y was derived from C(1)DX attached-X parental females rather than from C(1)RM attached-X parental females. Though the heterochromatic imprinting mechanism is unknown, a mutated Heterochromatin Protein 1 (HP1) gene, which is associated with suppression of position-effect variegation, increases expression of the w+ locus in the P[w+]YAL insert, indicating that HP1 may play a role in Y chromosome packaging. Key words: Drosophila melanogaster, heterochromatin, HP1, imprinting, P-element, Y chromosome.

scholarly journals The enhancer of position-effect variegation of Drosophila, E(var)3-93D, codes for a chromatin protein containing a conserved domain common to several transcriptional regulators

1993 ◽  
Vol 90 (23) ◽  
pp. 11376-11380 ◽  
Author(s):  
R Dorn ◽  
V Krauss ◽  
G Reuter ◽  
H Saumweber
Keyword(s):  
Position Effect ◽  
Polytene Chromosomes ◽  
Transcriptional Regulators ◽  
Molecular Data ◽  
Open Chromatin ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Effect Variegation ◽  
Gene Complexes ◽  
Broad Complex

In Drosophila modifying mutations of position-effect variegation have been successfully used to genetically dissect chromatin components. The enhancer of position-effect variegation E(var)3-93D [formerly E-var(3)3] encodes proteins containing a domain common to the transcriptional regulators tramtrack and the products of the Broad complex. It interacts with a number of chromatin genes that suppress position-effect variegation. Mutations in E(var)3-93D exhibit an imprinting-like effect on the Y chromosome. This effect is transmitted paternally over several generations. Homeotic transformations in E(var)3-93D mutants indicate an involvement of the gene products in regulation of homeotic gene complexes. An antiserum raised against E(var)3-93D protein detects this chromosomal protein in a large subset of sites in polytene chromosomes. Our genetic and molecular data suggest that the proteins of E(var)3-93D are generally involved in establishing and/or maintaining an open chromatin conformation.

scholarly journals Mutational Analysis of a Histone Deacetylase in Drosophila melanogaster: Missense Mutations Suppress Gene Silencing Associated With Position Effect Variegation

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 657-668 ◽  
Author(s):  
Randy Mottus ◽  
Richard E Sobel ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Histone Deacetylase ◽  
Transcriptional Activity ◽  
Mutational Analysis ◽  
Position Effect ◽  
Transcriptional Regulator ◽  
Position Effect Variegation ◽  
Missense Mutations ◽  
Effect Variegation ◽  
New Mutations

Abstract For many years it has been noted that there is a correlation between acetylation of histones and an increase in transcriptional activity. One prediction, based on this correlation, is that hypomorphic or null mutations in histone deacetylase genes should lead to increased levels of histone acetylation and result in increased levels of transcription. It was therefore surprising when it was reported, in both yeast and fruit flies, that mutations that reduced or eliminated a histone deacetylase resulted in transcriptional silencing of genes subject to telomeric and heterochromatic position effect variegation (PEV). Here we report the first mutational analysis of a histone deacetylase in a multicellular eukaryote by examining six new mutations in HDAC1 of Drosophila melanogaster. We observed a suite of phenotypes accompanying the mutations consistent with the notion that HDAC1 acts as a global transcriptional regulator. However, in contrast to recent findings, here we report that specific missense mutations in the structural gene of HDAC1 suppress the silencing of genes subject to PEV. We propose that the missense mutations reported here are acting as antimorphic mutations that “poison” the deacetylase complex and propose a model that accounts for the various phenotypes associated with lesions in the deacetylase locus.

scholarly journals Competition Between Different Variegating Rearrangements for Limited Heterochromatic Factors in Drosophila melanogaster

Genetics ◽  
1997 ◽  
Vol 145 (4) ◽  
pp. 945-959
Author(s):  
Vett K Lloyd ◽  
Donald A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Rearrangement ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Euchromatic Region ◽  
Single Chromosome ◽  
Mosaic Expression ◽  
Effect Variegation ◽  
Protein Components

Position effect variegation (PEV) results from the juxtaposition of a euchromatic gene to heterochromatin. In its new position the gene is inactivated in some cells and not in others. This mosaic expression is consistent with variability in the spread of heterochromatin from cell to cell. As many components of heterochromatin are likely to be produced in limited amounts, the spread of heterochromatin into a normally euchromatic region should be accompanied by a concomitant loss or redistribution of the protein components from other heterochromatic regions. We have shown that this is the case by simultaneously monitoring variegation of a euchromatic and a heterochromatic gene associated with a single chromosome rearrangement. Secondly, if several heterochromatic regions of the genome share limited components of heterochromatin, then some variegating rearrangements should compete for these components. We have examined this hypothesis by testing flies with combinations of two or more different variegating rearrangements. Of the nine combinations of pairs of variegating rearrangements we studied, seven showed nonreciprocal interactions. These results imply that many components of heterochromatin are both shared and present in limited amounts and that they can transfer between chromosomal sites. Consequently, even nonvariegation portions of the genome will be disrupted by re-allocation of heterochromatic proteins associated with PEV. These results have implications for models of PEV.

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