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Mismatch-repair signature mutations activate gene enhancers across human colorectal cancer epigenomes

ABSTRACT: Mismatch-repair signature mutations activate gene enhancers across human colorectal cancer epigenomes

PROVIDER: PRJNA521260 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8541250.fastq.gz	Fastqsanger.gz
	SRR8541260.fastq.gz	Fastqsanger.gz
	SRR8541251.fastq.gz	Fastqsanger.gz
	SRR8541261.fastq.gz	Fastqsanger.gz
	SRR8541252.fastq.gz	Fastqsanger.gz

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Mismatch-repair signature mutations activate gene enhancers across human colorectal cancer epigenomes

Project description:We show that mismatch-repair (MMR) signature mutations can activate colorectal cancer (CRC)-specific enhancers, through analysis of enhancer DNA associated with the active enhancer histone mark H3K27ac. We demonstrate that MMR mutations activate enhancers using a xenograft metastasis model, where mutations are induced naturally via CRISPR/Cas9 inactivation of MLH1 prior to tumor cell injection.

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Mismatch repair-signature mutations activate gene enhancers across human colorectal cancer epigenomes.

Project description:Commonly-mutated genes have been found for many cancers, but less is known about mutations in cis-regulatory elements. We leverage gains in tumor-specific enhancer activity, coupled with allele-biased mutation detection from H3K27ac ChIP-seq data, to pinpoint potential enhancer-activating mutations in colorectal cancer (CRC). Analysis of a genetically-diverse cohort of CRC specimens revealed that microsatellite instable (MSI) samples have a high indel rate within active enhancers. Enhancers with indels show evidence of positive selection, increased target gene expression, and a subset is highly recurrent. The indels affect short homopolymer tracts of A/T and increase affinity for FOX transcription factors. We further demonstrate that signature mismatch-repair (MMR) mutations activate enhancers using a xenograft tumor metastasis model, where mutations are induced naturally via CRISPR/Cas9 inactivation of MLH1 prior to tumor cell injection. Our results suggest that MMR signature mutations activate enhancers in CRC tumor epigenomes to provide a selective advantage.

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Project description:Mismatch repair protein coordinate with SETD2 to activate DNA oxidative damage response and repair in human cells

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Project description:The mismatch repair (MMR) family is a highly conserved group of proteins that function in correcting base-base and insertion-deletion mismatches generated during DNA replication. To systematically investigate the mismatch repair pathway, we conducted a proteomic analysis and identified MMR-associated protein complexes using a tandem-affinity purification coupled with mass spectrometry (TAP-MS) method. In total, we identified 262 high-confidence candidate interaction proteins (HCIPs).

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Project description:There is mounting evidence that mismatch repair (MMR) proteins are involved in oxidative DNA damage response. SETD2, the histone H3K36 tri-methyltransferase, is a newly found factor participate in MMR pathway in human cells. In this study, we show that SETD2 can directly interact with MMR protein MutSα, and they are enriched and colocalized in chromatin in response to oxidative damage, which maybe the reason for the amplification of H3K36me3. Moreover, MutSα and SETD2 are essential for ATM and CHK2 activation upon H2O2 treatment, loss of SETD2 and MutSα will display impaired DNA damage response and oxidative DNA repair, which will accumulate oxidative damage and lead to more cell apoptosis and cell death. Our finding provided a novel SETD2 dependent mechanism for the oxidative DNA damage response together with MMR protein.

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