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Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

ABSTRACT: Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

PROVIDER: PRJNA602514 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10919734.fastq.gz	Fastqsanger.gz
	SRR10919735.fastq.gz	Fastqsanger.gz
	SRR10919736.fastq.gz	Fastqsanger.gz
	SRR10919737.fastq.gz	Fastqsanger.gz
	SRR10919738.fastq.gz	Fastqsanger.gz

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Disruption of the MSL complex inhibits tumor maintenance by exacerbating chromosomal instability

Project description:Identification of gene expression changes induced after loss of a functional MSL complex in Transformed Dermal Fibroblast cells. Identification of copy number changes induced after loss of a functional MSL complex in Transformed Dermal Fibroblast cells.

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Disruption of the MSL complex inhibits tumour maintenance by exacerbating chromosomal instability.

Project description:Rewiring of cellular programmes in malignant cells generates cancer-specific vulnerabilities. Here, using an unbiased screening strategy aimed at identifying non-essential genes required by tumour cells to sustain unlimited proliferative capacity, we identify the male-specific lethal (MSL) acetyltransferase complex as a vulnerability of genetically unstable cancers. We find that disruption of the MSL complex and consequent loss of the associated H4K16ac mark do not substantially alter transcriptional programmes but compromise chromosome integrity and promote chromosomal instability (CIN) that progressively exhausts the proliferative potential of cancer cells through a p53-independent mechanism. This effect is dependent on pre-existing genomic instability, and normal cells are insensitive to MSL disruption. Using cell- and patient-derived xenografts from multiple cancer types, we show that excessive CIN induced by MSL disruption inhibits tumour maintenance. Our findings suggest that targeting MSL may be a valuable means to increase CIN beyond the level tolerated by cancer cells without inducing severe adverse effects in normal tissues.

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Genome-wide profiling of RNA associated to the MSL-complex in Drosophila melanogaster

Project description:In Drosophila, the global increase in transcription from the X chromosome in males to compensate for its monosomy is mediated by the male-specific-lethal complex (MSL-C) consisting of five proteins and two non-coding RNAs, roX1 and roX2. After an initial sequence dependent recognition by the MSL-C of 150-300 high affinity sites, the spreading to the majority of the X-linked genes depends on local MSL-C concentration and active transcription. Here we ask whether any additional RNA species are associated to the MSL-C. No additional roX were found but a strong association was found between the msl2 mRNA and the MSL-C. Based on our results we propose a model in which a non-chromatin associated partial or complete MSL-C titrates newly transcribed msl2 mRNA and thus feed-back regulates the amount of available MSL-C.

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Halanaerobium saccharolyticum strain:MSL 7

Project description:Halanaerobium saccharolyticum MSL 7 genome sequencing

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Project description:Halanaerobium saccharolyticum MSL 17.2 genome sequencing

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Halanaerobium saccharolyticum strain:MSL 19.2

Project description:Halanaerobium saccharolyticum MSL 19.2 genome sequencing

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Genome-wide profiling of RNA associated to the MSL-complex in Drosophila melanogaster

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Drosophila MSL complex selectively identifies active genes on the male X chromosome

Project description:X-chromosome dosage compensation in Drosophila requires the male-specific lethal (MSL) complex, which up-regulates gene expression from the single male X chromosome. Here, we define X-chromosome-specific MSL binding at high resolution in two male cell lines and in late-stage embryos. We find that the MSL complex is highly enriched over most expressed genes, with binding biased toward the 3' end of transcription units. The binding patterns are largely similar in the distinct cell types, with ~600 genes clearly bound in all three cases. Genes identified as clearly bound in one cell type and not in another indicate that attraction of MSL complex correlates with expression state. Thus, sequence alone is not sufficient to explain MSL targeting. We propose that the MSL complex recognizes most X-linked genes, but only in the context of chromatin factors or modifications indicative of active transcription. Distinguishing expressed genes from the bulk of the genome is likely to be an important function common to many chromatin organizing and modifying activities. Keywords: ChIP-chip

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