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

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

ORGANISM(S): Perkinsus marinus Nematostella vectensis Escherichia coli Mus musculus Daphnia pulex Strongylocentrotus purpuratus Haloferax mediterranei Creolimax fragrantissima Dryas iulia Capsaspora owczarzaki Sphaeroforma arctica Dictyostelium discoideum

PROVIDER: GSE223913 | GEO | 2024/02/05

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

RNA Pol II pausing facilitates phased pluripotency transitions by buffering transcription

Project description: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

2022-02-28 | GSE196543 | 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

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

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

Mus musculus

Project description:Wnt & LIF signalling in mESC

| PRJNA106143 | ENA

RNAPII interactome in INTS6 degron cells

Project description:In this study we show that acute INTS6 depletion remodels the RNAPII interactome and enhances ARMC5 binding, the same as what we observed in Ints6 KO cells. To investigate how acute INTS6 depletion affects RNAPII function, we determined the RNAPII interactome in the the Ints6 degron cells. Chromatin fractions from DMSO and dTAG treated Ints6 degron cells (treated for 1 hour) were analyzed by RNAPII IP-mass spectrometry. There are 12 samples in this MS run, samples 6-dTAG repeats1-3 and 6-DMSO repeats 1-3 are involved in the paper.

2025-12-22 | PXD053351 | Pride

LIF signaling-dependent gene expression

Project description:Leukemia Inhibitory Factor (LIF) plays an essential role in the maintenance of pluripotency of mouse embryonic stem cells (mESCs). LIF withdrawal induces mESC differentiation. To define noval pluripotent factors downstream of LIF signaling, cDNA microarray was used and seveal well-known pluripotent genes were found to respond to LIF withdrawal, including Klf4, Esrrb, Tbx3, and Prdm14.

2015-06-23 | GSE70104 | GEO

Degron models: a toolbox for rapid in vivo depletion of essential proteins regulating mRNA metabolism

Project description:Due to their essentiality, studying proteins involved in fundamental processes in vivo is challenging. PROTAC-based systems offer time-controlled protein depletion, but their characterization in vivo remains limited. Here, with an efficient direct zygote editing protocol, we generated degron-tag models (dTAG/FKBP or BromoTag) for seven genes involved in therapeutic and endogenous mRNA metabolism (Cnot1, Pan2, Tent5a, Tent4b, Dcp2, Rnasel, Tsg101). Degron tags occasionally caused phenotypes that were often mitigated by tag position or tagging system change. In cells, both approaches yielded rapid and sustained degradation. In mice, dTAG depletion was effective but varied by protein and administration route, whereas BromoTag showed no in vivo activity. We showcase the utility of these models through an analysis of CNOT1's roles in cell division, immunity, and poly(A) tail maintenance. We present a valuable toolbox for studying mRNA metabolism in mammalian models, while providing a benchmark for applying degron-tag models to study other biological processes.

2026-02-26 | PXD069282 | Pride

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