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Homo sapiens

ABSTRACT: Measuring the effect of MYC on transcription during the DNA double-strand break response by RNA-seq of newly synthesized transcripts

PROVIDER: PRJNA395319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5857020_1.fastq.gz	Fastqsanger.gz
	SRR5857020_2.fastq.gz	Fastqsanger.gz
	SRR5857021_1.fastq.gz	Fastqsanger.gz
	SRR5857021_2.fastq.gz	Fastqsanger.gz
	SRR5857022_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Measuring the effect of MYC on transcription during the DNA double-strand break response by RNA-seq of newly synthesized transcripts

Project description:We sequenced newly synthesized mRNA to determine which genes are differentially transcribed during the DNA double-strand break (DSB) response. Moreover, as the transcription factor MYC is repressed in a p53-dependent manner during the DSB response, we determined the effect of this repression on transcription by maintaining MYC above its basal expression level. To control for differences in cell size, we spiked in S. pombe RNA proportional to cell number, then normalized human transcript counts to S. pombe transcript counts. We found that ~77% of transcripts were produced at a lower level during the time interval 2.5‑3.5 h after treatment with neocarzinostatin (NCS), which causes DSBs, than in a one-hour time interval without NCS treatment. When MYC was maintained above its basal level during the DSB response, only ~59% of transcripts were produced at a lower level in NCS-treated cells. Known p53 target genes were upregulated during the same time interval, and maintaining MYC above its basal level did not change this significantly. Consistent with previous observations, we found that increasing MYC levels increased transcription of most genes, with a larger effect on more highly transcribed genes. We observed the opposite in NCS-treated cells, in which more highly transcribed genes were downregulated to a greater degree. These data support a model that p53, by repressing MYC, redistributes transcription during the DSB response, inhibiting global transcription while activating transcription of specific genes involved in the response.

2017-08-02 | GSE101738 | GEO

Ubiquitin-dependent transfer of PAF1c from MYC onto RNA Polymerase controls double-strand break repair at active promoters

Project description:MYC family proteins are oncogenic transcription factors that can globally affect the function of RNA Polymerase II (RNAPII). The ability of MYC proteins to promote transcription elongation depends on their ubiquitination, but the underlying mechanism and its biological relevance are unknown. Here we show that MYC and the Polymerase II associated factor, PAF1c, interact directly and their function is mutually dependent, since the specific binding of MYC to active promoters depends on PAF1c and, conversely, PAF1c is required for MYC-dependent pause release. Upon binding, PAF1c is rapidly transferred from MYC onto RNAPII and this transfer is driven by the HUWE1 ubiquitin ligase. Both MYC and HUWE1 globally control histone H2B ubiquitylation, which promotes transcriptional elongation and alters chromatin structure for double-strand break repair. Consistently, MYC suppresses the accumulation of double-strand breaks at promoters in response to topoisomerase II inhibition. While depletion of PAF1c has only minor effects on MYC-dependent gene expression, MYC induces rampant transcription-dependent DNA damage in PAF1c-depleted cells. We propose that the HUWE1-dependent transfer of PAF1c from MYC onto RNAPII is critical for absorbing the topological stress accompanied with deregulated and oncogenic transcription.

2021-02-15 | PXD023242 | Pride

p53 binding during the DNA double-strand break response

Project description:We used ChIP-seq to assess where p53 binds in the human genome and how that binding changes during the DNA double-strand break response. In particular, we considered the 1-Mb-wide window centered on the MYC locus. Contrary to previous reports, we found no evidence of p53 binding at the MYC promoter. Rather, we identified three locations downstream of MYC at which p53 was bound; binding at each of these regions increased during the DNA double-strand break response.

2017-08-02 | GSE101737 | GEO

MYC multimers shield stalled replication forks from RNA polymerase

Project description:Oncoproteins of the MYC family drive the development of numerous human tumors. In unperturbed cells, MYC proteins bind to virtually all active promoters and control transcription by RNA Polymerase II (RNAPII). MYC proteins can also coordinate transcription with DNA replication and promote the repair of transcription-associated DNA damage, but how they exert these mechanistically diverse functions is unknown. Here we show that MYC dissociates from many of its binding sites in active promoters and forms multimeric, often sphere-like structures in response to perturbation of transcription elongation, mRNA splicing or inhibition of the proteasome. Multimerization is accompanied by a global change in the MYC interactome towards proteins involved in transcription termination and RNA processing. MYC multimers accumulate on chromatin immediately adjacent to stalled replication forks and surround FANCD2, ATR and BRCA1 proteins, which are located at stalled forks. MYC multimerization is triggered in a HUWE1- and ubiquitylation-dependent manner. At active promoters, MYC multimers block antisense transcription and stabilize FANCD2 association with chromatin. This limits DNA double-strand break formation during S phase, suggesting that multimerization of MYC enables tumor cells to proliferate under stressful conditions.

2022-10-27 | PXD036674 | Pride

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters

| PRJNA631530 | ENA

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_W11)

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_W11)

| PRJNA631524 | ENA

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_DS)

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_DS)

| PRJNA631521 | ENA

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_RRL)

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_RRL)

| PRJNA631523 | ENA

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_MycER)

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_MycER)

| PRJNA631522 | ENA

Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_MycAID)

Project description:Ubiquitylation of MYC couples transcription elongation with double-strand break repair at active promoters (ChIPseq_TE_MycAID)

| PRJNA631525 | ENA

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