scholarly journals MATERNAL-ZYGOTIC LETHAL INTERACTIONS IN DROSOPHILA MELANOGASTER: THE EFFECTS OF DEFICIENCIES IN THE ZESTE-WHITE REGION OF THE X CHROMOSOME

Genetics ◽  
1980 ◽  
Vol 96 (1) ◽  
pp. 187-200 ◽  
Author(s):  
Leonard G Robbins
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Position Effect ◽  
Gene Activity ◽  
Position Effect Variegation ◽  
White Region ◽  
Effect Variegation ◽  
Zygotic Gene ◽  
Maternal Gene

ABSTRACT The possibility that essential loci in the zeste-white region of the Drosophila melanogaster X chromosome are expressed both maternally and zygotically has been tested. Maternal gene activity was varied by altering gene dose, and zygotic gene activity was manipulated by use of position-effect variegation of a duplication. Viability is affected when both maternal and zygotic gene activity are reduced, but not when either maternal or zygotic gene activity is normal. Tests of a set of overlapping deficiencies demonstrate that at least three sections of the zeste-white region yield maternal zygotic lethal interactions. Single-cistron mutations at two loci in one of these segments have been tested, and maternal heterozygosity for mutations at both loci give lethal responses of mutant-duplication zygotes. Thus, at least four of the 13 essential functions coded in the zeste-white region are active both maternally and zygotically, suggesting that a substantial fraction of the genome may function at both stages. The normal survival of zygotes when either maternal gene expression or zygotic gene expression is normal, and their inviability when both are depressed, suggests that a developmental stage exists when maternally determined functions and zygotically coded functions are both in use.

scholarly journals MATERNAL-ZYGOTIC LETHAL INTERACTIONS IN DROSOPHILA MELANOGASTER: ZESTE-WHITE REGION SINGLE-CISTRON MUTATIONS

Genetics ◽  
1983 ◽  
Vol 103 (4) ◽  
pp. 633-648
Author(s):  
Leonard G Robbins
Keyword(s):  
Position Effect ◽  
Gene Activity ◽  
Position Effect Variegation ◽  
Gene Products ◽  
Developmental Sequence ◽  
White Region ◽  
Number Of Genes ◽  
Effect Variegation ◽  
Zygotic Gene ◽  
Minimum Estimate

ABSTRACT Thirty-eight mutations in 13 essential loci in the zeste-white region were tested for interacting maternal and zygotic gene activity. Maternal mutant heterozygosity provided a partial maternal defect and position-effect variegation was used to alter the level of zygotic gene activity. This method yields a minimum estimate of the number of genes for which zygotic development depends upon both gene products stored in the egg and gene products synthesized in the zygote. Lethal interactions were found for one or more alleles at 10 of the 13 loci. The implications of these observations with respect to gene regulation and developmental sequence are considered.

Evidence for intrinsic differences in the formation of chromatin domains in Drosophila melanogaster.

Genetics ◽  
1992 ◽  
Vol 132 (4) ◽  
pp. 1063-1069 ◽  
Author(s):  
C P Bishop
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Genetic Background ◽  
Position Effect ◽  
The Other ◽  
Position Effect Variegation ◽  
Compaction Process ◽  
Chromatin Domains ◽  
Effect Variegation ◽  
Reporter Systems

Abstract The results of an investigation into intrinsic differences in the formation of two different heterochromatic domains are presented. The study utilized two different position effect variegation mutants in Drosophila melanogaster for investigating the process of compacting different stretches of DNA into heterochromatin. Each stretch of DNA encodes for a gene that affects different aspects of bristle morphology. The expression of each gene is prevented when it is compacted into heterochromatin thus the genes serve as effective reporter systems to monitor the spread of heterochromatin. Both variegating mutants are scored in the same cell such that environmental and genetic background differences are unambiguously eliminated. Any differences observed in the repression of the two genes must therefore be the result of intrinsic differences in the heterochromatic compaction process for the two stretches of DNA. Studies of the effects different enhancers of variegation have upon the compaction of the two genes indicate each compaction event occurs independently of the other, and that different components are involved in the two processes. These results are discussed with regard to spreading heterochromatin and the role this process may play in regulating gene expression.

Position-effect variegation in Drosophila melanogaster X chromosome inversion with a breakpoint in a satellite block and its suppression in a secondary rearrangement

Chromosoma ◽  
1998 ◽  
Vol 106 (8) ◽  
pp. 520-525 ◽  
Author(s):  
Eugene V. Tolchkov ◽  
Irina A. Kramerova ◽  
Sergei A. Lavrov ◽  
Vanya I. Rasheva ◽  
Silvia Bonaccorsi ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Chromosome Inversion ◽  
Effect Variegation ◽  
Secondary Rearrangement

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 Weakener of white (Wow), a gene that modifies the expression of the white eye color locus and that suppresses position effect variegation in Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 137 (4) ◽  
pp. 1057-1070 ◽  
Author(s):  
J A Birchler ◽  
U Bhadra ◽  
L Rabinow ◽  
R Linsk ◽  
A T Nguyen-Huynh
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Position Effect ◽  
Northern Analysis ◽  
Regulatory Sequences ◽  
Position Effect Variegation ◽  
Eye Color ◽  
Effect Variegation ◽  
Modifying Effect ◽  
Color Gene

Abstract A locus is described in Drosophila melanogaster that modifies the expression of the white eye color gene. This trans-acting modifier reduces the expression of the white gene in the eye, but elevates the expression in other adult tissues. Because of the eye phenotype in which the expression of white is lessened but not eliminated, the newly described locus is called the Weakener of white (Wow). Northern analysis reveals that Wow can exert an inverse or direct modifying effect depending upon the developmental stage. Two related genes, brown and scarlet, that are coordinately expressed with white, are also affected by Wow. In addition, Wow modulates the steady state RNA level of the retrotransposon, copia. When tested with a white promoter-Alcohol dehydrogenase reporter. Wow confers the modifying effect to the reporter, suggesting a requirement of the white regulatory sequences for mediating the response. In addition to being a dosage sensitive regulator of white, brown, scarlet and copia, Wow acts as a suppressor of position effect variegation. There are many dosage sensitive suppressors of position effect variegation and many dosage-sensitive modifiers of gene expression. The Wow mutations provide evidence for an overlap between the two types of modifiers.

scholarly journals Genomic Imprinting and Position-Effect Variegation in Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1503-1516 ◽  
Author(s):  
Vett K Lloyd ◽  
Don A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Genomic Imprinting ◽  
X Chromosome ◽  
Position Effect ◽  
Specific Effect ◽  
Position Effect Variegation ◽  
Mitotic Instability ◽  
Effect Variegation ◽  
Allele Specific ◽  
The Individual

Abstract Genomic imprinting is a phenomenon in which the expression of a gene or chromosomal region depends on the sex of the individual transmitting it. The term imprinting was first coined to describe parent-specific chromosome behavior in the dipteran insect Sciara and has since been described in many organisms, including other insects, plants, fish, and mammals. In this article we describe a mini-X chromosome in Drosophila melanogaster that shows genomic imprinting of at least three closely linked genes. The imprinting of these genes is observed as mosaic silencing when the genes are transmitted by the male parent, in contrast to essentially wild-type expression when the same genes are maternally transmitted. We show that the imprint is due to the sex of the parent rather than to a conventional maternal effect, differential mitotic instability of the mini-X chromosome, or an allele-specific effect. Finally, we have examined the effects of classical modifiers of position-effect variegation on the maintenance and the establishment of the imprint. Factors that modify position-effect variegation alter the somatic expression but not the establishment of the imprint. This suggests that chromatin structure is important in maintenance of the imprint, but a separate mechanism may be responsible for its initiation.

scholarly journals Observations on the induction of position effect variegation of euchromatic genes in Drosophila melanogaster.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 231-242
Author(s):  
G V Pokholkova ◽  
I V Makunin ◽  
E S Belyaeva ◽  
I F Zhimulev
Keyword(s):  
Drosophila Melanogaster ◽  
Low Temperature ◽  
X Chromosome ◽  
Position Effect ◽  
Complete Disappearance ◽  
Position Effect Variegation ◽  
Normal Phenotype ◽  
Normal Expression ◽  
Effect Variegation ◽  
Heterochromatic Sequence

Abstract In the T(1;2)dorvar7 translocation, the 1A-2B7-8 segment of the X chromosome is brought to the vicinity of 2R-chromosome heterochromatin resulting in position effect variegation of dor, BR-C and more distal genes, as well as compaction of chromatin in this segment. By irradiation of T(1;2)dorvar7, nine reversions (rev) to a normal phenotype were recovered. In two cases (rev27, rev226), the 1A-2B7-8 section is relocated to the 19A region of the X chromosome, forming free duplications (1A-2B7-8/19A-20F-X-het). Modifiers of position effect do not change the normal expression of the BR-C and dor genes in these duplications. In five reversions (rev3, rev40, rev60, rev167, rev175), free duplications have formed from the 1A-2B7-8 fragment and X chromosome heterochromatin. In these rearrangements, modifiers of position effect (low temperature, removal of Y and 2R-chromosome heterochromatin and a genetic enhancer (E-var(3)201) induce position-effect again. Two reversions (rev45 and rev110) are associated with additional inversions in the original dorvar7 chromosomes. The inversions relocate part of the heterochromatin adjacent to the 1A-2B7-8 section into new positions. In T(1;2)dorrev45, position-effect is seen in the 2B7-8-7A element as compaction spreading from 2B7-8 proximally in some cases as far as the 5D region. Thus, in rev45 the pattern of euchromatin compaction is reciprocal to that of the initial dorvar7 strain. Apparently, it is due to the same variegation-evoking center near the 2R centromere in both cases. In all nine revertants, weakening or complete disappearance of the position-effect is observed despite retention of the 20-kb heterochromatic segment adjacent to the 1A-2B7-8 region. Thus, a 20-kb heterochromatic sequence does not inactivate euchromatin joined to it.

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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