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Genome-wide gene and small RNA expression analysis of Y-chromosome aneuploidy strains of Drosophila melanogaster

ABSTRACT: Genome-wide gene and small RNA expression analysis of Y-chromosome aneuploidy strains of Drosophila melanogaster

PROVIDER: PRJNA361573 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5181410_1.fastq.gz	Fastqsanger.gz
	SRR5181410_2.fastq.gz	Fastqsanger.gz
	SRR5181420_1.fastq.gz	Fastqsanger.gz
	SRR5181420_2.fastq.gz	Fastqsanger.gz
	SRR5181430.fastq.gz	Fastqsanger.gz

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Genome-wide gene expression analysis of Y-chromosome aneuploidy strains of Drosophila melanogaster

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Aneuploidy tolerance caused by BRG1 loss allows gain of chromosome 18 and improved fitness

Project description:Aneuploidy results in decreased cellular fitness in many different species and model systems. However, aneuploidy is commonly found in cancer cells and often correlates with aggressive growth and poor prognosis, suggesting that the impact of aneuploidy on cellular fitness is context dependent. The BRG1 (SMARCA4) subunit of the SWI/SNF chromatin remodelling complex is a tumour suppressor that is frequently lost in cancer cells. Here, we used a chromosomally stable cell line to test the effect of BRG1 loss on the evolution of aneuploidy. We find that BRG1 deletion leads to an initial loss of fitness in this cell line that improves over time. The improved fitness correlates with a gain of extra copies of chromosome 18. Notably, changes in pathways that are known to promote tolerance to aneuploidy are evident immediately upon loss of BRG1, providing an environment where karyotype changes associated with a fitness advantage can be explored. At least in some genetic backgrounds, therefore, loss of the SWI/SNF complex can contribute to tumourigenesis through tolerance of aneuploidy.

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Loss of the SUMO Protease Ulp2 Triggers a Specific Multi-Chromosome Aneuploidy

Project description:Post-translational protein modification by the small ubiquitin-related modifier (SUMO) protein regulates numerous cellular pathways, including transcription, cell division and genome maintenance. The SUMO protease Ulp2 modulates many of these SUMO-dependent processes in budding yeast. To investigate changes to the transcriptome of cells lacking Ulp2, whole-genome RNA sequencing (RNA-seq) was employed. Unexpectedly, ulp2Δ cells display a general two-fold increase in transcript levels across two particular chromosomes, Chromosome I (ChrI) and Chromosome XII (ChrXII). Quantification of relative DNA levels showed that ChrI and ChrXII are present at twice their normal copy number in ulp2Δ cells. This double disomy occurs in mutants in multiple genetic backgrounds and does not require passage through meiosis. An abnormal number of chromosomes in a cell, termed aneuploidy, is usually deleterious. However, development of specific aneuploidies allows rapid adaptation to cellular stresses in yeast and other species, and aneuploidy characterizes most tumors. Extra copies of ChrI and ChrXII appear quickly following loss of active Ulp2, suggesting aneuploidy is an adaptive mechanism in cells lacking the functional SUMO protease. The specific aneuploidy in ulp2Δ cells highlights a unique example of a homogeneous, multi-chromosome aneuploidy in response to mutation of a single gene.

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