Stable polymorphism for mutant eye colour geues in populations of Drosophila melanogaster in two different media

Genetica ◽  
1988 ◽  
Vol 77 (2) ◽  
pp. 123-131 ◽  
Author(s):  
C. N�iera ◽  
J. L. M�nsua
Keyword(s):  
Drosophila Melanogaster ◽  
Eye Colour

Genetic location and biochemical characterization of eye-colour mutants from natural populations of Drosophila melanogaster

Genome ◽  
1990 ◽  
Vol 33 (2) ◽  
pp. 203-208 ◽  
Author(s):  
M. Luisa Aparisi ◽  
Carmen Nájera
Keyword(s):  
Drosophila Melanogaster ◽  
Biochemical Characterization ◽  
Natural Populations ◽  
High Variability ◽  
Genetic Location ◽  
Eye Colour ◽  
Different Seasons ◽  
Allelism Tests ◽  
Mutation And Selection

From six captures of Drosophila melanogaster carried out in three different habitats (cellar, vineyard, and pinewood) in two different seasons of the year (spring and autumn), 60 eye-colour mutations were isolated, which were reduced to 29 loci by means of allelism tests within and between populations. Forty-five of these mutations were analyzed genetically and biochemically; of these 33 turned out to be previously described mutants and mapped to a total of 17 loci. Twelve new mutants were discovered and they mapped to 12 new loci, distributed on chromosomes X, II, and III. The eye-colour mutants show large effects on the red and brown pigments. The high variability of the eye-colour loci is discussed in relation to the mutation and selection hypotheses.Key words: eye-colour mutants, variability, mapping, Drosophila melanogaster, pigment patterns.

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.

Two Unusual Modifications of Eye Colour in Drosophila melanogaster

Nature ◽  
1936 ◽  
Vol 138 (3482) ◽  
pp. 165-166
Author(s):  
E. V. ENZMANN ◽  
C. P HASKINS
Keyword(s):  
Drosophila Melanogaster ◽  
Eye Colour

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

2020 ◽  
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.

scholarly journals Experiments with the maroon-like mutation of Drosophila melanogaster

1977 ◽  
Vol 29 (2) ◽  
pp. 159-170 ◽  
Author(s):  
Moti Nissani ◽  
Chih-Ping Liu
Keyword(s):  
Drosophila Melanogaster ◽  
Developmental Stages ◽  
Cell Lineage ◽  
Nutritional Deficiencies ◽  
Chromosome Loss ◽  
Negative Results ◽  
Eye Colour ◽  
Colour Development ◽  
The One

SUMMARYCell lineage analysis of the maroon-like mutation of Drosophila melanogaster revealed the most extensive degree of non-autonomy reported to date in Drosophila: all 1454 gynandromorphs in which X chromosome loss uncovered the ma-l mutation had ma-l+. eye colour. In contrast, among 331 gynandromorphs in which X chromosome loss simultaneously uncovered the vermilion and maroon-like mutations, approximately 16% had v phenotype but with one possible exception all gynandromorphs again had ma-l+ eye colour. These results suggest that very small amounts of the ma-l+ gene product are necessary for wild-type eye colour development and they are therefore compatible with the one cistron–allelic complementation model that has been proposed for the ma-l locus. They also provide the best estimate available to date of In(1)wvc-induced internal mosaicism: 7%. A preliminary attempt to detect DNA-induced transformants among 6 DNA-injected preblastoderm ma-l embryos and at least 80000 of their F1 to F4 descendants has yielded completely negative results. An investigation of the maternal effect which ma-l+ mothers exert on the eye colour of their genetically ma-l offspring revealed that, in contrast to earlier observations, this effect is not universal: some phenotypically ma-l and intermediate ma-l flies were observed in young cultures. The discrepancy between this and earner observations is probably attributable to as yet uncharacterized nutritional deficiencies in the diet of flies used in this experiment. Cytoplasm drawn from blastoderm ma-l+ embryos and injected into the posterior region of ma-l preblastoderm embryos failed to induce eye-colour alterations in all seven flies which survived the treatment. Injection of the contents of embryos of certain genotypes and developmental stages into ma-l pupae 24–48 h old did alter in some instances the eye colour of treated ma-l flies. Various tests strongly suggest that these alterations are not due to injection of a substance that has been stored in the egg during oogensis or that has been produced by the embryo itself prior to injection and they therefore preclude the possibility that a simple in vivo bioassay for the ma-l+ substance has been achieved. Rather, they indicate that the observed eye-colour alterations are due to transplantation of blastoderm-stage embryos which remain active long enough within ma-l hosts to produce and release a substance into the hosts' haemolymph and that this substance in turn induces phenotypic alterations in the hosts' eye colour. When v and ma-l eye colour changes are simultaneously monitored, it appears that injection of embryonic contents into pupae is equally or more effective in modifying the v phenotype than in modifying the ma-l phenotype. Based on these observations, a tentative hypothesis regarding the time of activation of the ma-l+ gene and the relationship between the immediate product of this gene, the maternal substance stored in the egg and the substance released by tissue transplants is proposed.

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