Delineating functional enhancers (cis-regulome) in LPS-activated murine splenic B cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121753 | GEO | 2019/12/23
REPOSITORIES: GEO
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Project description:Delineating functional enhancers (cis-regulome) in LPS-activated murine splenic B cells
| PRJNA498316 | ENA
Project description:Naïve CD4+ T Cells are capable of differentiating into numerous T helper effector lineages depending on the provided local cytokines during activation. Cis-regulatory elements (CRE) are critical for cell differentiation, homeostasis, and function; however, CRE functional annotation (e.g. silencers, enhancers, and insulators) from existing genomic libraries remains an active need. Genome wide screens, including Transcribing Active Regulatory Region Sequencing (STARR-Seq) provides quantifies enhancer activity. However, these screens are mainly conducted in immortalized cell lines. Therefore, we have modified STARR-Seq using a non-integrating lentiviral transduction system (Lenti-STARR-seq) to investigate CRE in human CD4+ T cells. We identify and validate functional enhancers and negative regulatory elements (NRE). These elements differences stark differences in chromatin modification, TF binding, and nucleosome positioning. Additionally, STARR-Seq enhancers, but not NRE, exhibit transcription of enhancer RNA. Collectively these data suggest that Lenti-STARR-Seq may be a useful tool in the screening of primary human cell types for CRE function, and provides an atlas of functional CRE in human CD4+ T Cells.
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Project description:Multiple myeloma (MM) is a hematological cancer with inevitable drug resistance. MM cells interacting with bone marrow stromal cells (BMSCs) undergo substantial changes in transcriptome and develop de novo drug resistance. As a critical component in transcriptional regulation, how chromatin landscape is transformed in MM cells and regulates the transcriptional response to BMSCs remains elusive. We profiled transcriptome and regulome for MM cells using a transwell coculture system with BMSCs. The transcriptome and regulome of MM cells from the upper transwell resembled MM cells coexisting with BMSCs from the lower chamber but were distinctive to monoculture. BMSC-induced genes were enriched in JAK2/STAT3 signaling pathway, unfolded protein stress, signatures of early plasma cells, and response to proteasome inhibitors. Genes with accessibility increased at multiple regulatory sites were preferentially induced by BMSCs and enriched in response to drug and unfavorable prognostic markers from several MM patient cohorts. We proposed JUNB and ATF4::CEBPβ as candidate transcription factors (TFs) that modulated the BMSC-induced transformation of regulome linked to the response to external stimuli. Together, we characterized BMSC-induced transcriptome and regulome signatures of MM cells and prioritized TFs for future study to depict epigenetic mechanisms of BMSC-induced drug resistance in MM.
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Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT NK cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control.
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Project description:ChIP-seq was conducted using freshly isolated (resting) splenic WT CD8+ T cells with anti-Runx3 antibody (Ab), anti-H3K4me1 Ab and non-immune serum (NIS) as control.
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Project description:To quantify functional enhancers, we performed STARR-seq (Self-Transcribing Active Regulatory Region sequencing) in the U2OS-GR and the U2OS-AR cell lines (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for rat GR or human AR, respectively). U2OS-GR cells were treated with dexamethasone (1 µM) or vehicle (ethanol) for 14 hours. U2OS-AR cells were treated with R1881 (5 nM) or vehicle (DMSO) for 14 hours. To limit the number of putative enhancers, the STARR library contained genomic regions isolated by FAIRE (Formaldehyde Assisted Isolation of Regulatory Elements) from dexamethasone-treated U2OS-GR cells to include regions that gain accessibility upon GR activation. We added unique molecular identifiers (UMIs) during the reverse transcription stage to facilitate quantitative measurements of enhancer activity for each fragment. The UMI for each read is present within the sequence identifier line (directly following the y coordinate and separated by a ':') of the fastq files.
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Project description:Precise spatiotemporally regulated gene expression is pivotal for cell homeostasis, cell differentiation and during development. Gene expression networks are tightly regulated by transcription factors (TF) and their targeted regulatory genomic elements (enhancers), which are known to correlate with specific histone modifications. However, the ultimate prerequisites, which determine functionally active enhancers, remain unclear. To elucidate the regulatory landscape of murine ESCs, a massively parallel reporter assay, based on STARR-seq (Self-Transcribing Active Regulatory Region sequencing), assessing genomic fragments prepared from accessible chromatin, (FAIRE-STARR-seq) has been applied. Thus, a genome-wide quantitative map of functional mESC enhancers in naive state and after retinoic acid (RA)-induced differentiation was generated. To investigate sequence features associated with RA-mediated inducibility of enhancers bound by retinoic acid receptor alpha (RARα), the main receptor for RA, genomic binding sites of RARα have been determined.
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