Unknown,Transcriptomics,Genomics,Proteomics

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Brn2 (POU3F2) ChIP-seq data obtained from asynchronous or mitotically arrested mouse neural stem/progenitor cells

ABSTRACT: dataset contains 8 samples: 2 asynchronous and 2 mitotically synchronized populations (one with 90% and another with 95% mitotic purity) and 4 corresponding inputs. Cells were synchonized for 10h with colchicine at 330nM. asyncronous samples (interphase) were sonicated and prepared in parallel with same cell number as the corresponding mitotic samples. Fetal neural stem/progenitor cells were obtained from mouse telencephalon (ventral region) at E13.5. This data generated 4 genome-wide binding profiles corresponding to Brn2 (POU3f2) binding sites, aligned to MM9 mus musculus dataset.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Diogo Castro

PROVIDER: E-MTAB-9758 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Recognition of modified histones by “reader” proteins plays a critical role in the regulation of transcription1. H3K36 trimethylation (H3K36me3) is deposited onto the nucleosomes in the transcribed regions following RNA polymerase II (Pol II) elongation. In yeast, this mark in turn recruits epigenetic regulators to reset the chromatin at an appropriate state to suppress cryptic transcription2,3. However, much less is known about the role of H3K36me3 in transcription regulation in mammals. This is further complicated by the transcription-coupled incorporation of the histone variant H3.3 in gene bodies4. Here we show that the candidate tumor suppressor ZMYND11 specifically recognizes H3K36me3 on H3.3 (H3.3K36me3) and regulates Pol II elongation. Structural studies reveal that in addition to the trimethyl-lysine binding by an aromatic cage within the PWWP domain, the H3.3-dependent recognition is mediated by the encapsulation of the H3.3-specific “Ser31” residue in a composite pocket formed by the tandem bromo-PWWP domains of ZMYND11. ChIP-sequencing analysis reveal a genome-wide colocalization of ZMYND11 with H3K36me3 and H3.3 in gene bodies, and its occupancy requires the pre-deposition of H3.3K36me3. Although ZMYND11 is associated with highly expressed genes, it functions as an unconventional transcription corepressor via modulating the transition of the promoter-proximal paused Pol II to elongation. ZMYND11 is critical for the repression of a transcriptional program that is essential for tumor cell growth; higher expression of ZMYND11 is observed in triple-negative breast cancer patients with better prognosis. Consistently, overexpression of ZMYND11 suppresses cancer cell growth and tumor formation in mice. Together, this study identifies ZMYND11 as an H3.3-specific reader of H3K36me3 that links the histone variant-mediated transcription elongation control to tumor suppression. ChIP-seq analysis of ZMYND11, H3K36me3 in U2OS cells and ZMYND11 knockdown cells; ChIP-seq of H3.3 in Flag-H3.3 stable U2OS cells; RNA-seq of ZNYMD11 depleted U2OS cells.

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Brn2 (POU3F2) ChIP-seq data obtained from asynchronous or mitotically arrested mouse neural stem/progenitor cells

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