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RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

ABSTRACT: ChIP-seq experiments of NELFB (HA), NELFE, and Spt5 in mESCs under serum/LIF conditions. The experiments where performed with and without dTAG degradation of NELFB

ORGANISM(S): Mus musculus

PROVIDER: GSE196543 | GEO | 2022/02/28

REPOSITORIES: GEO

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RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

Project description:PRO-seq experiment of Nelfb deg mESC in serum/LIF or during pluripotency transitions, with or without dTAG-13.

2022-02-16 | GSE196653 | GEO

Pol II pausing is a milestone on the road to complex animals

Project description:PRO-seq experiments in multiple organisms. Also, PRO-seq experiment of Nelfb and Nelfe degron mESC in serum/LIF with or without dTAG-13.

2024-02-05 | GSE223913 | GEO

Rapid and efficient adaptation of the dTAG system in mammalian development reveals stage specific requirements of NELF

Project description:mRNA expression profile of late 2-cell mouse embryos cultured +/- dTAG-13 to degrade NELFB from the zygote stage.

2022-02-19 | GSE185099 | GEO

RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

Project description:RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

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RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

Project description:RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

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The Integrator complex controls the termination of transcription at diverse classes of gene targets

Project description:Complexes containing INTS3 and either NABP1 or NABP2 were initially characterized in DNA damage responses, but their biochemical function remained unknown. Using affinity purifications and HIV Integration Targeting-Sequencing (HIT-Seq), we find that these complexes are part of the Integrator complex, which binds RNA Polymerase II and regulates specific target genes. Integrator cleaves snRNAs as part of their processing to their mature form in a mechanism that is intimately coupled with transcription termination. However, HIT-Seq reveals that Integrator also binds to the 3’ end of replication-dependent histones and promoter proximal regions of genes with polyadenylated transcripts. Depletion of Integrator subunits results in transcription termination failure, disrupting histone mRNA processing, and leading to polyadenylation of snRNAs and histone mRNAs. Furthermore, promoter proximal binding of Integrator negatively regulates expression of genes whose transcripts are normally polyadenylated. Integrator recruitment to all three gene classes is DSIF-dependent, suggesting that Integrator functions as a termination complex at DSIF-dependent RNA Polymerase II pause sites. HITseq was used to interrogate chromatin binding sites of of proteins in the complex (including INIP, INTS3, INTS9, INTS11, NABP1, NABP2, NELFA, NELFB, NELFCD, NELFE, SPT5). These proteins were fused to LEDGF-IBD and expressed in mouse LEDGF-/-MEF cells. The fusion proteins then target HIV integration to the chromatin binding sites. The HIV integration sites were identified using linker-mediated PCR and highthroughput sequencing and serve as surrogate for chromatin binding sites. Mapping was done using mouse genome mm9.

2015-01-20 | E-GEOD-65090 | biostudies-arrayexpress

RNA Polymerase II Pausing Factor NELF in CD8+ T Cells Promotes Anti-Tumor Immunity

Project description:The master transcriptional regulator T cell factor 1 (TCF1) is required for the anti-tumor functions of memory and stem-like CD8+ T cells. However, how TCF1 partners with other transcription factors to orchestrate the gene activation program critical for anti-tumor immunity remains poorly understood. Here we show that negative elongation factor B (NELFB), an RNA polymerase II pausing factor, cooperates with TCF1 in T cell responses to cancer. Genetic ablation of mouse Nelfb in mature T lymphocytes severely impaired anti-tumor immunity responding to both primary tumor challenge and tumor antigen-mediated vaccination. NELFB depletion resulted in more exhausted, and reduced memory, T cell populations, whereas its ectopic expression boosted host anti-tumor immunity and efficacy of chimeric antigen receptor (CAR) T-cell immunotherapy. Mechanistically, NELFB is physically associated with TCF1 and recruited preferentially to TCF1-enriched transcriptional enhancers and promoters in CD8+ T cells. Nelfb ablation significantly restricted chromatin accessibility to these TCF1-associated loci. Thus, NELFB is a previously unrecognized functional partner of TCF1 that potentiates the chromatin openness of TCF1-targeting regulatory elements. Our findings also suggest that augmenting NELFB expression in CD8+ T cells may improve therapeutic outcomes of anti-cancer CAR-T immunotherapies.

2022-03-19 | GSE182862 | GEO

Essential Signaling Function of Cytoplasmic NELFB Independent of RNA Polymerase II Pausing

Project description:Biochemical studies have established that the four-subunit negative elongation factor (NELF) complex mediates RNA polymerase II (Pol II) pausing at promoter proximal regions. Genetic ablation of individual NELF subunits destabilizes the entire NELF complex and causes lethality of cultured cells, leading to the prevailing concept that NELF-mediated Pol II pausing is essential for cell survival. Using separation-of-function mutations, we show here that NELFB’s effects on cell proliferation can be uncoupled from its function in Pol II pausing. NELFB mutants localized in the cytoplasm and incapacitated in the NELF complex assembly still retain their ability to support cell proliferation and at least part of NELFB-dependent transcriptome. Furthermore, we demonstrate that cytoplasmic NELFB physically and functionally interacts with multiple pro-survival signaling kinases, most notably PI3K/AKT. Enforced activation of PI3K/AKT-related kinases largely rescues deficiency of NELFB-depleted cells in proliferation, but not Pol II pausing. Together, these data revise the current understanding of the growth impact of Pol II pausing and underscore multiplicity of the biological function of individual NELF subunits.

2023-06-30 | GSE205388 | GEO

Essential Signaling Function of Cytoplasmic NELFB Independent of RNA Polymerase II Pausing [ChIP-seq]

2023-06-30 | GSE205504 | GEO

Transcription Pausing Regulates Mouse Embryonic Stem Cell Differentiation [GRO-seq]

Project description:The pluripotency of embryonic stem cells (ESCs) relies on appropriate responsiveness to developmental cues. Promoter-proximal pausing of RNA polymerase II (Pol II) has been suggested to play a role in keeping genes poised for future activation. To identify the role of Pol II pausing in regulating ESC pluripotency, we have generated mouse ESCs carrying a mutation in the pause-inducing factor SPT5. Consistent with previous in vitro studies showing the pausing deficiency of this mutant SPT5, our genomic analysis reveals genome-wide reduction of paused Pol II in mutant mESCs. Furthermore, we find that genes differentially regulated by mutant SPT5 correlates with distinct chromatin states. Functionally, this pausing-deficient SPT5 disrupts ESC differentiation without affecting self-renewal. Thus, our study uncovers an important role of Pol II pausing in regulating ESC differentiation and also suggests that Pol II pausing can both positively and negatively influence transcription depending on the local chromatin environment.

2017-12-08 | GSE99747 | GEO

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