scholarly journals Characterization of sequences associated with position-effect variegation at pericentric sites in Drosophila heterochromatin

Chromosoma ◽  
1998 ◽  
Vol 107 (5) ◽  
pp. 277-285 ◽  
Author(s):  
Diane E. Cryderman ◽  
Matthew H. Cuaycong ◽  
Sarah C. R. Elgin ◽  
Lori L. Wallrath
Keyword(s):  
Position Effect ◽  
Position Effect Variegation ◽  
Effect Variegation ◽  
Drosophila Heterochromatin

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 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 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.

pitkinD, a Novel Gain-of-Function Enhancer of Position-Effect Variegation, Affects Chromatin Regulation During Oogenesis and Early Embryogenesis in Drosophila

Genetics ◽  
2001 ◽  
Vol 157 (3) ◽  
pp. 1227-1244 ◽  
Author(s):  
Steffi Kuhfittig ◽  
János Szabad ◽  
Gunnar Schotta ◽  
Jan Hoffmann ◽  
Endre Máthé ◽  
...  
Keyword(s):  
Germ Line ◽  
Position Effect ◽  
Early Embryogenesis ◽  
Position Effect Variegation ◽  
Chromatin Regulation ◽  
Gain Of Function ◽  
Position Effects ◽  
Dominant Female ◽  
Effect Variegation ◽  
Female Germ Line

Abstract The vast majority of the >100 modifier genes of position-effect variegation (PEV) in Drosophila have been identified genetically as haplo-insufficient loci. Here, we describe pitkinDominant (ptnD), a gain-of-function enhancer mutation of PEV. Its exceptionally strong enhancer effect is evident as elevated spreading of heterochromatin-induced gene silencing along euchromatic regions in variegating rearrangements. The ptnD mutation causes ectopic binding of the SU(VAR)3-9 heterochromatin protein at many euchromatic sites and, unlike other modifiers of PEV, it also affects stable position effects. Specifically, it induces silencing of white+ transgenes inserted at a wide variety of euchromatic sites. ptnD is associated with dominant female sterility. +/+ embryos produced by ptnD/+ females mated with wild-type males die at the end of embryogenesis, whereas the ptnD/+ sibling embryos arrest development at cleavage cycle 1-3, due to a combined effect of maternally provided mutant product and an early zygotic lethal effect of ptnD. This is the earliest zygotic effect of a mutation so far reported in Drosophila. Germ-line mosaics show that ptn+ function is required for normal development in the female germ line. These results, together with effects on PEV and white+ transgenes, are consistent with the hypothesis that the ptn gene plays an important role in chromatin regulation during development of the female germ line and in early embryogenesis.

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.

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