Mosaic suppressor, a gene in Drosophila that modifies retrotransposon expression and interacts with zeste.

Genetics ◽  
1994 ◽  
Vol 136 (2) ◽  
pp. 573-583
Author(s):  
A K Csink ◽  
R Linsk ◽  
J A Birchler
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Low Frequency ◽  
Transcript Abundance ◽  
White Gene ◽  
Copia Retrotransposon ◽  
Transcriptional Units ◽  
Regulatory Effects

Abstract A newly identified locus in Drosophila melanogaster, Mosaic suppressor (Msu), is described. This gene modifies the expression of white-apricot (wa), which is a copia retrotransposon-induced allele of the white gene. In addition to suppressing wa in a mosaic fashion, this mutation suppresses or enhances the expression of several other retrotransposon induced white alleles. Mutations in Msu alter copia transcript abundance and may regulate the expression of several other retrotransposons. While each of the two Msu isolates is homozygous lethal, heteroallelic escapers occur at a low frequency. These escapers act not only as strong suppressors of wa, but also as a recessive enhancer of synaptic-dependent gene expression at white. The mutation described here suggests a connection between the regulation of specific transcriptional units such as retrotransposons and more global synapsis dependent regulatory effects.

scholarly journals Identification of mutations in three genes that interact with zeste in the control of white gene expression in Drosophila melanogaster.

Genetics ◽  
1994 ◽  
Vol 138 (3) ◽  
pp. 733-739
Author(s):  
P G Georgiev
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Dna Sequences ◽  
Binding Sites ◽  
Null Allele ◽  
White Gene ◽  
Long Distance ◽  
Protein Binding Sites ◽  
White Locus ◽  
White Mutant

Abstract Three previously described genes, enhancer of yellow, 1, 2 and 3, are shown to cooperate with the zeste gene in the control of white gene expression. The mutations e(y)1u1, e(y)3u1, and to a lesser extent e(y)2u1, enhance the effect of the zeste null allele zv77h. Different combinations of e(y)1u1, e(y)2u1 and e(y)3u1 mutations with several other z alleles also enhance the white mutant phenotype, but only to levels characteristic of white alleles containing a deletion of the upstream eye enhancer. Loss of zeste protein binding sites from the white locus does not eliminate the effect of e(y)1u1 and e(y)3u1 mutations, suggesting that the products of these genes interact with some other nucleotide sequences. Combinations of either e(y)1u1 or e(y)2u1 mutations with e(y)3u1 are lethal. The products of these three genes may represent, together with zeste, a group of proteins involved in the organization of long-distance interactions between DNA sequences.

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 ◽  
White Gene ◽  
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 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 to 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.

Post-Transcriptional Regulation of Cardiac Sarcomere Protein Titin Through 3’ Untranslated Regions

2013 ◽  
Vol 9 ◽  
Author(s):  
Tara A Shrout
Keyword(s):  
Gene Expression ◽  
Transcriptional Control ◽  
Striated Muscle ◽  
Binding Capacity ◽  
Structural Features ◽  
Neonatal Rat ◽  
Regulatory Control ◽  
Untranslated Regions ◽  
Luciferase Reporter ◽  
Regulatory Effects

Titin is the largest known protein in the human body, and forms the backbone of all striated muscle sarcomeres. The elastic nature of titin is an important component of muscle compliance and functionality. A significant amount of energy is expended to synthesize titin, thus we postulate that titin gene expression is under strict regulatory control in order to conserve cellular resources. In general, gene expression is mediated in part by post-transcriptional control elements located within the 5’ and 3’ untranslated regions (UTRs) of mature mRNA. The 3’UTR in particular contains structural features that affect binding capacity to other RNA components, such as MicroRNA, which control mRNA localization, translation, and degradation. The degree and significance of the regulatory effects mediated by two determined variants of titin’s 3’ UTR were evaluated in Neonatal Rat Ventricular Myocyte and Human Embryonic Kidney cell lines. Recombinant plasmids to transfect these cells lines were engineered by insertion of the variant titin 3’UTR 431- and 1047-base pairs sequences into luciferase reporter vectors. Expression due to an unaltered reporter vector served as the control. Quantitative changes in luciferase activity due to the recombinants proportionally represented the effect titin’s respective 3’UTR conferred on downstream post-transcriptional expression relative to the control. The effect due to titin’s shorter 3’UTR sequence was inconclusive; however, results illustrated that titin’s longer 3’UTR sequence caused a 35 percent decrease in protein expression. Secondary structural analysis of the two sequences revealed differential folding patterns that affect the stability and degree of MicroRNA-binding within titin’s variant 3’UTR sequences.

Study of Dosage Compensation in Drosophila

Genetics ◽  
2003 ◽  
Vol 165 (3) ◽  
pp. 1167-1181
Author(s):  
Pei-Wen Chiang ◽  
David M Kurnit
Keyword(s):  
Gene Expression ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Qpcr Assay ◽  
Male And Female ◽  
Multiple Genes ◽  
Chromosomal Changes ◽  
Regulatory Effects

Abstract Using a sensitive RT-QPCR assay, we analyzed the regulatory effects of sex and different dosage compensation mutations in Drosophila. To validate the assay, we showed that regulation for several genes indeed varied with the number of functional copies of that gene. We then confirmed that dosage compensation occurred for most genes we examined in male and female flies. Finally, we examined the effects on regulation of several genes in the MSL pathway, presumed to be involved in sex-dependent determination of regulation. Rather than seeing global alterations of either X chromosomal or autosomal genes, regulation of genes on either the X chromosome or the autosomes could be elevated, depressed, or unaltered between sexes in unpredictable ways for the various MSL mutations. Relative dosage for a given gene between the sexes could vary at different developmental times. Autosomal genes often showed deranged regulatory levels, indicating they were in pathways perturbed by X chromosomal changes. As exemplified by the BR-C locus and its dependent Sgs genes, multiple genes in a given pathway could exhibit coordinate regulatory modulation. The variegated pattern shown for expression of both X chromosomal and autosomal loci underscores the complexity of gene expression so that the phenotype of MSL mutations does not reflect only simple perturbations of genes on the X chromosome.

scholarly journals Multi-Locus Selection and the Structure of Variation at the white Gene of Drosophila melanogaster

Genetics ◽  
1996 ◽  
Vol 144 (2) ◽  
pp. 635-645 ◽  
Author(s):  
David A Kirby ◽  
Wolfgang Stephan
Keyword(s):  
Drosophila Melanogaster ◽  
White Gene ◽  
Transcriptional Unit ◽  
North American Population ◽  
Evolutionary Mechanisms ◽  
Locus Selection ◽  
Neutral Equilibrium ◽  
History Of ◽  
High Degree ◽  
Very High

Abstract We surveyed sequence variation and divergence for the entire 5972-bp transcriptional unit of the white gene in 15 lines of Drosophila melanogaster and one line of D. simulans. We found a very high degree of haplotypic structuring for the polymorphisms in the 3′ half of the gene, as opposed to the polymorphisms in the 5′ half. To determine the evolutionary mechanisms responsible for this pattern, we sequenced a 1612-bp segment of the white gene from an additional 33 lines of D. melanogaster from a European and a North American population. This 1612-bp segment encompasses an 834bp region of the white gene in which the polymorphisms form high frequency haplotypes that cannot be explained by a neutral equilibrium model of molecular evolution. The small number of recombinants in the 834bp region suggests epistatic selection as the cause of the haplotypic structuring, while an investigation of nucleotide diversity supports a directional selection hypothesis. A multi-locus selection model that combines features from both-hypotheses and takes the recent history of D. melanogaster into account may be the best explanation for these data.

scholarly journals Comparative approaches to the study of physiology: Drosophila as a physiological tool

2013 ◽  
Vol 304 (3) ◽  
pp. R177-R188 ◽  
Author(s):  
Wendi S. Neckameyer ◽  
Kathryn J. Argue
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Pattern Formation ◽  
Signaling Pathways ◽  
Human Disease ◽  
Cognitive Disorders ◽  
Model System ◽  
Critical Questions ◽  
Developmental Signaling ◽  
Shed Light

Numerous studies have detailed the extensive conservation of developmental signaling pathways between the model system, Drosophila melanogaster, and mammalian models, but researchers have also profited from the unique and highly tractable genetic tools available in this system to address critical questions in physiology. In this review, we have described contributions that Drosophila researchers have made to mathematical dynamics of pattern formation, cardiac pathologies, the way in which pain circuits are integrated to elicit responses from sensation, as well as the ways in which gene expression can modulate diverse behaviors and shed light on human cognitive disorders. The broad and diverse array of contributions from Drosophila underscore its translational relevance to modeling human disease.

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