scholarly journals A cytogenetic analysis of chromosomal region 31 of Drosophila melanogaster.

Genetics ◽  
1993 ◽  
Vol 134 (1) ◽  
pp. 221-230 ◽  
Author(s):  
N J Clegg ◽  
I P Whitehead ◽  
J K Brock ◽  
D A Sinclair ◽  
R Mottus ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosomal Region ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Recessive Lethal ◽  
Chromosomal Proteins ◽  
Complementation Groups ◽  
New Alleles ◽  
Dominant Suppressor ◽  
New Mutations

Abstract Cytogenetic region 31 of the second chromosome of Drosophila melanogaster was screened for recessive lethal mutations. One hundred and thirty nine new recessive lethal alleles were isolated that fail to complement Df(2L)J2 (31A-32A). These new alleles, combined with preexisting mutations in the region, define 52 complementation groups, 35 of which have not previously been described. Among the new mutations were alleles of the cdc2 and mfs(2)31 genes. Six new deficiencies were also isolated and characterized identifying 16 deficiency subintervals within region 31. The new deficiencies were used to further localize three loci believed to encode non-histone chromosomal proteins. Suvar(2)1/Su(var)214, a dominant suppressor of position-effect variegation (PEV), maps to 31A-B, while the recessive suppressors of PEV mfs(2)31 and wdl were localized to regions 31E and 31F-32A, respectively. In addition, the cytological position of several mutations that interact with heterochromatin were more precisely defined.

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 GENETIC ANALYSIS OF THE ANTENNAPEDIA GENE COMPLEX (ANT-C) AND ADJACENT CHROMOSOMAL REGIONS OF DROSOPHILA MELANOGASTER. II. POLYTENE CHROMOSOME SEGMENTS 84A–84B1,2

Genetics ◽  
1980 ◽  
Vol 95 (2) ◽  
pp. 383-397
Author(s):  
R A Lewis ◽  
B T Wakimoto ◽  
R E Denell ◽  
T C Kaufman
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Analysis ◽  
Normal Development ◽  
Chromosome 3 ◽  
Gene Complex ◽  
Functional Sites ◽  
Complementation Groups ◽  
Chromosome Segments ◽  
New Alleles ◽  
New Mutations

ABSTRACT The existence of a gene complex in the proximal right arm of chromosome 3 of Drosophila melanogaster involved in the development of the head and thorax was originally suggested by the phenotypes of several dominant homoeotic mutations and their revertants. A screen for mutations utilizing Df(3R) AntpNS+R17 (proximally broken in salivary region 84B1,2) yielded, among 102 recovered mutations, 17 localized by deficiency mapping to the putative homoeotic cluster. These fell into four complementation groups, two of which were characterized by homoeotic phenotypes. To explore the limits of the Antennapedia gene complex (ANT-C) more proximally, a second screen has been undertaken utilizing Df(3R)Scr, a deficiency of 84A1-B1,2.——Of 2832 chromosomes screened, 21 bearing alterations localized to polytene interval 84A-84B1,2 have been recovered. Sixteen are recessive lethals, and five showing reduced viability display a visible phenotype in surviving individuals. Complementation and phenotypic analyses revealed four complementation groups proximal to those identified in the previous screen, including two new alleles of the recessive homoeotic mutation, proboscipedia (pb). Ten of the new mutations correspond to complementation groups defined previously in the Df(3R)AntpNS+R17 screen, four to the EbR11 group, two to the Scr group and four to the Antp group.——On the basis of the phenotypes of the 39 mutations localized to this region, plus their interactions with extant homoeotic mutations, we postulate that there are at least five functional sites comprising the ANT-C. Three have been demonstrated to he homoeotic in nature. The specific homoeotic transformations thus far observed suggest that these loci are critical for normal development of adult labial, maxillary and thoracic structures.

scholarly journals A cytogenetic analysis of the Punch-tudor region of chromosome 2R in Drosophila melanogaster.

Genetics ◽  
1989 ◽  
Vol 121 (2) ◽  
pp. 273-280
Author(s):  
J O'Donnell ◽  
R Boswell ◽  
T Reynolds ◽  
W Mackay
Keyword(s):  
Drosophila Melanogaster ◽  
Cytogenetic Analysis ◽  
Deletion Mapping ◽  
Lethal Mutations ◽  
Complementation Groups ◽  
Chromosome Bands ◽  
New Alleles ◽  
New Mutations

Abstract Eleven chromosomal deficiencies and several rearrangements in the Pu-tud region of chromosome 2R have been generated and examined cytologically. The Pu locus has been localized to chromosome bands 57C5-6 and tud to 57C7-8. Mutagenesis within the region defined by the deletion intervals has resulted in the isolation of 92 new lethal mutations. Seventy-six of these mutations have been separated into 16 complementation groups that have been ordered and placed cytologically by deletion mapping. All new alleles fully complement tud for both lethal and grandchildless phenotypes. The largest number of new mutations, a total of 25, are Pu alleles.

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.

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.

A CYTOGENETIC ANALYSIS OF THE CHROMOSOMAL REGION SURROUNDING THE α-GLYCEROPHOSPHATE DEHYDROGENASE LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 371-386
Author(s):  
Michael A Kotarski ◽  
Sally Pickert ◽  
Ross J MacIntyre
Keyword(s):  
Drosophila Melanogaster ◽  
Polytene Chromosome ◽  
Cytogenetic Analysis ◽  
Chromosomal Region ◽  
Chromosome Band ◽  
Recombination Analysis ◽  
Chromosome 2 ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Glycerophosphate Dehydrogenase

ABSTRACT The chromosomal region surrounding the structural gene for α-glycerophosphate dehydrogenase (αGpdh, 2-20.5) of Drosophila melanogaster has been studied in detail. Forty-three EMS-induced recessive lethal mutations and five previously identified visible mutations have been localized within the 25A-27D region of chromosome 2 by deficiency mapping and in some cases by a recombination analysis. The 43 lethal mutations specify 17 lethal loci. ?Gpdh has been localized to a single polytene chromosome band, 25F5, and there apparently are no lethals that map to the αGpdh locus.

scholarly journals Transgenerational effect of drug-mediated inhibition of LSD1 on eye pigment expression in Drosophila

BMC Ecology ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Sigrid Hoyer-Fender
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Histone Modifications ◽  
Optical Measurement ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Drug Induced ◽  
Lysine Specific Demethylase ◽  
Eye Colour

Abstract Background The Drosophila melanogaster mutant white-mottled is a well-established model for position-effect variegation (PEV). Transposition of the euchromatic white gene into the vicinity of the pericentric heterochromatin caused variegated expression of white due to heterochromatin spreading. The establishment of the euchromatin-heterochromatin boundary and spreading of silencing is regulated by mutually exclusive histone modifications, i.e. the methylations of histone H3 at lysine 9 and lysine 4. Demethylation of H3K4, catalysed by lysine-specific demethylase LSD1, is required for subsequent methylation of H3K9 to establish heterochromatin. LSD1 is therefore essential for heterochromatin formation and spreading. We asked whether drug-mediated inhibition of LSD affects the expression of white and if this induced change can be transmitted to those generations that have never been exposed to the triggering signal, i.e. transgenerational epigenetic inheritance. Results We used the lysine-specific demethylase 1 (LSD1)-inhibitor Tranylcypromine to investigate its effect on eye colour expression in consecutive generations by feeding the parental and F1 generations of the Drosophila melanogaster mutant white-mottled. Quantitative Western blotting revealed that Tranylcypromine inhibits H3K4-demethylation both in vitro in S2 cells as well as in embryos when used as feeding additive. Eye colour expression in male flies was determined by optical measurement of pigment extracts and qRT-PCR of white gene expression. Flies raised in the presence of Tranylcypromine and its solvent DMSO showed increased eye pigment expression. Beyond that, eye pigment expression was also affected in consecutive generations including F3, which is the first generation without contact with the inhibitor. Conclusions Our results show that feeding of Tranylcypromine and DMSO caused desilencing of white in treated flies of generation F1. Consecutive generations, raised on standard food without further supplements, are also affected by the drug-induced alteration of histone modifications. Although eye pigment expression eventually returned to the basal state, the observed long-lasting effect points to a memory capacity of previous epigenomes. Furthermore, our results indicate that food compounds potentially affect chromatin modification and hence gene expression and that the alteration is putatively inherited not only parentally but transgenerationally.

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