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Buffering of segmental and chromosomal aneuploidies in Drosophila melanogaster

ABSTRACT: Chromosomal instability which involves deletion and duplication of chromosomes or chromosome parts is a common feature of cancers, and deficiency screens are commonly used as a method to find genes involved in different biological pathways. Still, how gene expression from whole chromosomes or large chromosomal domains is affected by deficiencies, duplications or chromosome loss is largely unknown. Using expression microarrays of deficiency hemizygotes and a duplication hemizygote we show that expressed genes are significantly buffered when present in a deficiency hemizygote and that the buffering effect is general and not mainly caused by feedback regulation of individual genes. Differentially expressed genes are in general better buffered than ubiquitously expressed genes when present in one copy. When present in three copies, differentially expressed genes are in general less buffered than ubiquitously expressed genes. Furthermore, we show that the 4th chromosome is compensated in response to dose differences. Our results suggest that general mechanisms exist to stimulate and to repress gene expression of aneuploidy regions and on the 4th chromosome this compensation is mediated by POF (Painting of Fourth). Keywords: dose response

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE14517 | GEO | 2009/03/30

SECONDARY ACCESSION(S): PRJNA111665

REPOSITORIES: GEO

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Transcription profiling of Drosophila deficiency hemizygotes and a duplication hemizygote reveals buffering of segmental and chromosomal aneuploidies in Drosophila melanogaster

Project description:Chromosomal instability which involves deletion and duplication of chromosomes or chromosome parts is a common feature of cancers, and deficiency screens are commonly used as a method to find genes involved in different biological pathways. Still, how gene expression from whole chromosomes or large chromosomal domains is affected by deficiencies, duplications or chromosome loss is largely unknown. Using expression microarrays of deficiency hemizygotes and a duplication hemizygote we show that expressed genes are significantly buffered when present in a deficiency hemizygote and that the buffering effect is general and not mainly caused by feedback regulation of individual genes. Differentially expressed genes are in general better buffered than ubiquitously expressed genes when present in one copy. When present in three copies, differentially expressed genes are in general less buffered than ubiquitously expressed genes. Furthermore, we show that the 4th chromosome is compensated in response to dose differences. Our results suggest that general mechanisms exist to stimulate and to repress gene expression of aneuploidy regions and on the 4th chromosome this compensation is mediated by POF (Painting of Fourth). Experiment Overall Design: We prepared total RNA from flies heterozygous for three different deletions, Df(2L)J-H, Df (2L)ED4470, Df(2L)ED4651, flies heterozygous for the duplication Dp(2;2)Cam3 and flies with only one chromosome 4, or three copies of the 4th chromosome, as well as from wild type control flies. Three biological replicates of all genotypes were prepared.

2009-04-03 | E-GEOD-14517 | biostudies-arrayexpress

Buffering and proteolysis are induced upon segmental haploidy in Drosophila melanogaster.

Project description:Aneuploidy, i.e., variation in the number of individual chromosomes (chromosomal aneuploidy) or chromosome segment (segmental aneuploidy) is associated with developmental abnormalities and reduced fitness in all species examined, is the leading cause of miscarriages and mental retardations and a hallmark of cancer. Despite their documented importance in disease the effects of aneuploidies on the transcriptome remains largely unknown. Here we have examined the expression output in seven deficiency heterozygotes as single deficiencies and in all pairwise combinations. The results show that genes in one copy are buffered, i.e., are expressed above the expected 50% expression level compared to wild type and the buffering is general and not influenced by additional haploid regions. Long genes are significantly better buffered than short genes and our analysis suggests that gene length is the primary determinant for the degree of buffering. For short genes the degree of buffering depends on expression level and expression pattern. Furthermore, the results show that in deficiency heterozygotes the expression of genes involved in proteolysis is enhanced and negatively correlates with the degree of buffering. Our results suggest that proteolysis is a general response induced by aneuploidy.

2012-04-05 | GSE34400 | GEO

Buffering and proteolysis are induced upon segmental haploidy in Drosophila melanogaster.

2012-04-04 | E-GEOD-34400 | biostudies-arrayexpress

Transcriptome profiling of wild type and Pof mutant Drosophila melanogaster females

Project description:In Drosophila, two chromosome-wide compensatory systems have been characterized; the dosage compensation system acting on the male X-chromosome and the chromosome specific regulation of genes located on the heterochromatic 4th chromosome. Dosage compensation in Drosophila is accomplished by hypertranscription of the single male X-chromosome mediated by the MSL-complex. The mechanism for this compensation is suggested to be an MSL-complex mediated enhanced transcriptional elongation while the mechanism for the compensation mediated by Painting of fourth (POF) on the 4th chromosome has remained elusive. Here we show that POF binds to nascent RNA and this binding is associated with an increase in amount of chromosome 4 transcripts. Furthermore, genes located on the 4th chromosome are enriched in binding of the nucleoplasmic nucleporin component NUP98 and this enrichment correlates to increased POF binding. We also show that genes located in heterochromatic regions have a shorter transition time from site of transcription and to the nuclear envelope. Our current work broadens the understanding about how genes in heterochromatic regions can overcome the repressive influence of their hostile environment.

2012-05-31 | GSE28513 | GEO

Genome-wide profiling of RNA associated to the chromosome 4 specific protein POF in Drosophila melanogaster

2012-05-31 | GSE28518 | GEO

ISAba1 mediated intrinsic chromosomal oxacillinase duplication conveys carbapenem resistance

Project description:Tandem duplication of carbapenemase genes amplifies the gene copy number and enhances carbapenem resistance. These amplifications are often heterogenous, transient, locate in plasmids, which often also contribute to heteroresistance. The duplication is especially important for low-hydrolysis activity enzymes, which is often overlooked or even under controversy. Here we reported an intrinsic oxacillinase duplication mediated by two neighbor ISAba1inserted in the same orientation. The duplication is relatively stable, located in chromosome, and the duplication times is up to twenty-five, much larger than previous reports. We provided genomic, transcriptomic, and proteomic evidence that the duplication resulted oxacillinase overproduction and thus contribute to carbapenem resistance. No other possible carbapenem resistance related changes (point mutations of oxaAb, disturbed expression of porin protein and efflux pump) were found during the duplication process. Furthermore, introducing oxaAb flanked by two ISAba1 to A. baumannii via plasmids, mimicked the in vivo duplication process under carbapenem stress. Taken together, ISAba1 mediated duplication of low activity intrinsic antibiotic hydrolysis enzymes could lead to antibiotic resistance for advanced-generation antibiotics.

2023-01-17 | PXD039528 | iProX

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Non-coding roX RNAs Prevent the Binding of the MSL-complex to Heterochromatic Regions

Project description:Long non-coding RNAs are involved in dosage compensation both in mammals and in Drosophila by inducing changes in the X-chromosome chromatin structure. In Drosophila melanogaster, roX1 and roX2 are long non-coding RNAs that together with proteins form the male-specific lethal (MSL) complex, which coats the entire male X-chromosome and mediates dosage compensation by increased transcriptional output. It has been shown that in polytene chromosomes, in absence of both roX1 and roX2, the MSL-complex is decreased on the male X-chromosome and found relocated to the chromocenter, and the 4th chromosome. Here we address the role of roX RNAs in MSL-complex targeting and in the evolution of dosage compensation in Drosophila. We performed ChIP-seq experiments and show that MSL-complex recruitment to high affinity sites (HAS) on the X-chromosome is independent on roX and that the HAS sequence motif is conserved in D. simulans. Additionally, a complete and enzymatically active MSL-complex is recruited to six specific genes on the 4th chromosome. Interestingly, our sequence analysis shows that in the absence of roX RNAs, the MSL-complex has affinity to regions enriched in Hoppel transposable elements and to repeats in general. We hypothesize that roX mutants reveal an ancient targeting of the MSL-complex and propose that the role of roX RNAs is to restrict MSL-complex from binding to heterochromatin.

2014-11-07 | GSE58768 | GEO

Chromatin IP of POF, HP1 and H3K9ac and transcript profiling in S2 cells and salivary glands

Project description:Two chromosome-targeting and gene regulatory systems are present in Drosophila melanogaster. The male X-chromosome is targeted by the male-specific lethal complex believed to mediate the two-fold up-regulation of the X-linked genes. The highly heterochromatic 4th chromosome is specifically targeted by the Painting of Fourth (POF) protein which together with heterochromatin protein 1 (HP1) modulate the expression level of genes on the 4th chromosome. Here we report high-resolution mapping of POF and HP1 on the 4th chromosome using chromatin immunoprecipitation followed by tiling microarrays (ChIP-chip) in S2 cells and salivary glands. The enrichments are compared to transcript profiles of the two cell types used. POF specifically binds to genes with a strong preference for exons. The POF binding profile correlates to the binding profile of HP1 which in addition displays a typical “peak” in the promoter regions of bound genes. POF and HP1 binds to active genes and the binding correlates with levels of transcription and changes in binding levels are paralleled by a comparable change in transcription. Our results provide a high resolution description of the chromosome 4 specific gene regulatory system provided by the combinatorial effects of POF and HP1. This SuperSeries is composed of the SubSeries listed below.

2007-10-03 | GSE8301 | GEO

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