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

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

PROVIDER: PRJNA688290 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13314132.fastq.gz	Fastqsanger.gz
	SRR13314133.fastq.gz	Fastqsanger.gz
	SRR13314134.fastq.gz	Fastqsanger.gz
	SRR13314135.fastq.gz	Fastqsanger.gz
	SRR13314136.fastq.gz	Fastqsanger.gz

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

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.

2022-07-06 | GSE163940 | GEO

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.

2019-02-07 | GSE126188 | GEO

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

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

| PRJNA521260 | ENA

TRIP assay of mismatch repair during single-strand annealing

Project description:Biases of DNA repair can shape the nucleotide landscape of genomes at evolutionary timescales. However, such biases have not yet been measured in chromatin for lack of technologies. Here we develop a genome-wide assay whereby the same DNA lesion is repaired in different chromatin contexts. We insert thousands of barcoded transposons carrying a reporter of DNA mismatch repair in the genome of mouse embryonic stem cells. Upon inducing a double-strand break between tandem repeats, a mismatch is generated when the single strand annealing repair pathway is used. Surprisingly, the mismatch repair machinery favors the same strand 60-80% of the time. The location of the lesion in the genome and the type of mismatch have little influence on the repair bias in this context.

2020-05-14 | GSE141211 | GEO

Transcriptomic evaluation of mismatch repair defects

Project description:Using numerous isogenic models of mismatch repair defects we sought to understand how these defects influence global transcription

2018-09-08 | GSE119667 | GEO

Transcriptomic evaluation of mismatch repair defects

Project description:Transcriptomic evaluation of mismatch repair defects

| PRJNA489879 | ENA

Human DNA Mismatch Repair pathway LC-MSMS

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).

2016-02-08 | PXD003014 | Pride

Human DNA Mismatch Repair pathway LC-MSMS

2016-03-13 | MSV000079578 | MassIVE

Mismatch repair gene sequencing of sebaceous neoplasia

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DNA mutagenesis driven by transcription factor competition with mismatch repair

Project description:The distribution of somatic mutations across the genome is not uniform. Recently, an unexpected pattern of hyper-mutation was reported at binding sites of transcriptional regulatory factors (TFs). In some human cells, a decrease in DNA repair activity was also observed at TF binding sites, leading to the hypothesis that TFs may increase mutagenesis by interfering with the recognition of DNA lesions by repair enzymes, and thus inhibiting repair. However, direct proof of this surprising TF-induced mutagenesis mechanism is lacking. Here, we show that TF binding to DNA mismatch lesions leads to increased mutation rates at TF binding sites by reducing the efficiency of lesion recognition by MutSα, the main enzyme that initiates mismatch repair in eukaryotic cells. We developed a yeast mutagenesis assay to directly observe the accumulation of mutations in a TF binding site. Upon TF overexpression, the binding site exhibited an increased mutation rate, specifically for mutations resulting from mismatches where the TF strongly reduced MutSα binding in vitro. This trend was amplified in cells with an increased rate of misincorporation errors, and it was not observed in mismatch repair-deficient cells. Analyses of human cancer somatic mutation data revealed a pattern similar to that observed in yeast, with mutations resulting from TF-bound mismatches being specifically enriched in mismatch repair-proficient tumors. Taken together, our results demonstrate that in addition to their well-known roles in gene regulation, TFs also play a role in DNA mutagenesis, by directly interfering with the repair of replication errors. Since a majority of cancer mutations originate from unrepaired replication errors, most commonly mismatches, our results suggest that TF interference with mismatch repair will shape the mutation landscape of regulatory DNA in cancer genomes.

2025-03-31 | GSE235855 | GEO

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