scholarly journals Recombinogenic Effects of Suppressors of Position-Effect Variegation in Drosophila

Genetics ◽  
2002 ◽  
Vol 160 (2) ◽  
pp. 609-621
Author(s):  
Thomas Westphal ◽  
Gunter Reuter
Keyword(s):  
Chromatin Structure ◽  
Position Effect ◽  
Heterochromatic Region ◽  
Crossing Over ◽  
Position Effect Variegation ◽  
Chromosome 2 ◽  
Additive Effects ◽  
Suppressor Mutations ◽  
Effect Variegation ◽  
Meiotic Nondisjunction

Abstract Compact chromatin structure, induction of gene silencing in position-effect variegation (PEV), and crossing-over suppression are typical features of heterochromatin. To identify genes affecting crossing-over suppression by heterochromatin we tested PEV suppressor mutations for their effects on crossing over in pericentromeric regions of Drosophila autosomes. From the 46 mutations (28 loci) studied, 16 Su(var) mutations of the nine genes Su(var)2-1, Su(var)2-2, Su(var)2-5, Su(var)2-10, Su(var)2-14, Su(var) 2-15, Su(var)3-3, Su(var)3-7, and Su(var)3-9 significantly increase in heterozygotes or by additive effects in double and triple heterozygotes crossing over in the ri-pp region of chromosome 3. Su(var)2-201 and Su(var) 2-1401 display the strongest recombinogenic effects and were also shown to enhance recombination within the light-rolled heterochromatic region of chromosome 2. The dominant recombinogenic effects of Su(var) mutations are most pronounced in proximal euchromatin and are accompanied with significant reduction of meiotic nondisjunction. Our data suggest that crossing-over suppression by heterochromatin is controlled at chromatin structure as well as illustrate the possible effects of heterochromatin on total crossing-over frequencies in the genome.

scholarly journals Mutations in the Drosophila melanogaster Gene Encoding S-adenosylmethionine Suppress Position-Effect Variegation

Genetics ◽  
1996 ◽  
Vol 143 (2) ◽  
pp. 887-896 ◽  
Author(s):  
Jan Larsson ◽  
Jingpu Zhang ◽  
Åsa Rasmuson-Lestander
Keyword(s):  
Drosophila Melanogaster ◽  
Chromatin Structure ◽  
Position Effect ◽  
Regulatory Region ◽  
Polycomb Group ◽  
Position Effect Variegation ◽  
Gene Encoding ◽  
Sex Combs ◽  
S Alleles ◽  
Effect Variegation

Abstract In Drosophila melanogaster, the study of trans-acting modifier mutations of position-effect variegation and Polycomb group (Pc-G) genes have been useful tools to investigate genes involved in chromatin structure. We have cloned a modifier gene, Suppesssm of zeste 5 (Su(z)5), which encodes Sadenosylmethionine synthetase, and we present here molecular results and data concerning its expression in mutants and genetic interactions. The mutant alleles Su(z)5, l(2)R23 and l(2)M6 show suppression of wm4 and also of two white mutants induced by roo element insertions in the regulatory region i.e., wis (in combination with z  1) and wsp1. Two of the Su(z)S alleles, as well as a deletion of the gene, also act as enhancers of PoZycomb by increasing the size of sex combs on midleg. The results suggest that Su(z)5 is connected with regulation of chromatin structure. The enzyme Sadenosylmethionine synthetase is involved in the synthesis of Sadenosylmethionine, a methyl group donor and also, after decarboxylation, a propylamino group donor in the bio-synthesis of polyamines. Our results from HPLC analysis show that in ovaries from heterozygous Su(z)5 mutants the content of spermine is significantly reduced. Results presented here suggest that polyamines are an important molecule class in the regulation of chromatin structure.

scholarly journals Telomeric Position Effect Variegation in Saccharomyces cerevisiae by Caenorhabditis elegans Linker Histones Suggests a Mechanistic Connection between Germ Line and Telomeric Silencing

2003 ◽  
Vol 23 (10) ◽  
pp. 3681-3691 ◽  
Author(s):  
Monika A. Jedrusik ◽  
Ekkehard Schulze
Keyword(s):  
Caenorhabditis Elegans ◽  
Chromatin Structure ◽  
Germ Line ◽  
Budding Yeast ◽  
Position Effect ◽  
Linker Histone ◽  
Position Effect Variegation ◽  
Linker Histones ◽  
C Elegans ◽  
Effect Variegation

ABSTRACT Linker histones are nonessential for the life of single-celled eukaryotes. Linker histones, however, can be important components of specific developmental programs in multicellular animals and plants. For Caenorhabditis elegans a single linker histone variant (H1.1) is essential in a chromatin silencing process which is crucial for the proliferation and differentiation of the hermaphrodite germ line. In this study we analyzed the whole linker histone complement of C. elegans by telomeric position effect variegation in budding yeast. In this assay an indicator gene (URA3) placed close to the repressive telomeric chromatin structure is subject to epigenetically inherited gene inactivation. Just one out of seven C. elegans linker histones (H1.1) was able to enhance the telomeric position effect in budding yeast. Since these results reflect the biological function of H1.1 in C. elegans, we suggest that chromatin silencing in C. elegans is governed by molecular mechanisms related to the telomere-dependent silencing in budding yeast. We confirmed this hypothesis by testing C. elegans homologs of three yeast genes which are established modifiers of the yeast telomeric chromatin structure (SIR2, SET1, and RAD17) for their influence on repeat-dependent transgene silencing for C. elegans.

scholarly journals Trans-inactivation of the Drosophila brown gene: evidence for transcriptional repression and somatic pairing dependence

1989 ◽  
Vol 86 (17) ◽  
pp. 6704-6708 ◽  
Author(s):  
S Henikoff ◽  
T D Dreesen
Keyword(s):  
Chromatin Structure ◽  
Transcriptional Repression ◽  
Position Effect ◽  
Structure Characteristic ◽  
Position Effect Variegation ◽  
Direct Transmission ◽  
Dominant Effect ◽  
Effect Variegation ◽  
Somatic Pairing ◽  
Structural Configurations

Position-effect variegation in Drosophila is the variable inactivation of a gene that occurs when it is juxtaposed to heterochromatic regions of chromosomes. The brown gene, required for pteridine pigment in the eye, is unusual in that expression of the unrearranged homolog also is affected. This dominant effect can be very strong, as inactivation is detectable when as many as three trans copies of the gene are present. We show that pteridine reductions coincide with similar reductions in the accumulation of brown mRNA. The dominant effect is suppressed by certain altered structural configurations of the brown region, suggesting that somatic pairing is involved in the phenomenon. We propose that direct transmission of the altered chromatin structure characteristic of position-effect variegation (heterochromatinization) occurs between paired homologs in the region of the brown locus.

scholarly journals A cytogenetic and genetic characterization of a group of closely linked second chromosome mutations that suppress position-effect variegation in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 130 (2) ◽  
pp. 333-344 ◽  
Author(s):  
D A Sinclair ◽  
A A Ruddell ◽  
J K Brock ◽  
N J Clegg ◽  
V K Lloyd ◽  
...  
Keyword(s):  
Position Effect ◽  
Position Effect Variegation ◽  
Chromosome 2 ◽  
Var Genes ◽  
Effect Variegation ◽  
Chromosome Mutations ◽  
Male Specific ◽  
Dose Dependent ◽  
Var Gene

Abstract Characterization of a group of dominant second chromosome suppressor of position-effect variegation (PEV) (Su(var)) mutants has revealed a variety of interesting properties, including: maternal-effect suppression of PEV, homozygous lethality or semilethality and male-specific hemizygous lethality, female infecundity, acute sensitivity to the amount of heterochromatin in the cell and sensitivity to sodium butyrate. Deficiency/duplication mapping and complementation tests have revealed that eight of the mutants define at least two genes in section 31 of the left arm of chromosome 2 and they suggest that a ninth corresponds to an additional nonessential Su(var) gene within or near this region. The effects of specific deficiencies and a duplication on PEV indicate that the expression of one or more of the Su(var) genes in this region of the chromosome is dose-dependent, i.e., capable of haplo-abnormal suppression and triplo-abnormal enhancement. Interestingly, the appearance of certain visible phenotypes among a subset of the mutants suggests that they may possess antimorphic properties. Our results are consistent with the hypothesis that two of these Su(var) genes encode structural components of heterochromatin. We also report that two previously isolated mutants located in 31E and 31F-32A act as recessive suppressors of PEV.

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.

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.

white+ Transgene Insertions Presenting a Dorsal/Ventral Pattern Define a Single Cluster of Homeobox Genes That Is Silenced by the Polycomb-group Proteins in Drosophila melanogaster

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 257-275 ◽  
Author(s):  
Sophie Netter ◽  
Marie-Odile Fauvarque ◽  
Ruth Diez del Corral ◽  
Jean-Maurice Dura ◽  
Dario Coen
Keyword(s):  
Chromatin Structure ◽  
Target Genes ◽  
Position Effect ◽  
Phenotypic Expression ◽  
Positional Information ◽  
Genomic Region ◽  
Polycomb Group ◽  
Position Effect Variegation ◽  
Trithorax Group ◽  
Clear Cut

AbstractWe used the white gene as an enhancer trap and reporter of chromatin structure. We collected white+ transgene insertions presenting a peculiar pigmentation pattern in the eye: white expression is restricted to the dorsal half of the eye, with a clear-cut dorsal/ventral (D/V) border. This D/V pattern is stable and heritable, indicating that phenotypic expression of the white reporter reflects positional information in the developing eye. Localization of these transgenes led us to identify a unique genomic region encompassing 140 kb in 69D1–3 subject to this D/V effect. This region contains at least three closely related homeobox-containing genes that are constituents of the iroquois complex (IRO-C). IRO-C genes are coordinately regulated and implicated in similar developmental processes. Expression of these genes in the eye is regulated by the products of the Polycomb -group (Pc-G) and trithorax-group (trx-G) genes but is not modified by classical modifiers of position-effect variegation. Our results, together with the report of a Pc -G binding site in 69D, suggest that we have identified a novel cluster of target genes for the Pc-G and trx-G products. We thus propose that ventral silencing of the whole IRO-C in the eye occurs at the level of chromatin structure in a manner similar to that of the homeotic gene complexes, perhaps by local compaction of the region into a heterochromatin-like structure involving the Pc-G products.

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