OEX_Cui-Cui_2311201516
Ontology highlight
ABSTRACT:
TISSUE(S): ['cell Line']
SUBMITTER: Cui-Cui Liu
PROVIDER: OEX00025490 | NODE | 2023-11-20
REPOSITORIES: NODE
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Project description:The type III secretion system (T3SS) is the main machinery for Pseudomonas syringae and other Gram-negative bacteria to invade plant cells. HrpR/HrpS heterodimer are key factors to activate HrpL which induces all T3SS genes by binding to a ‘hrp box’ in promoters. However, the molecular mechanisms of HrpRS on T3SS or non-T3SS genes have not been fully understood. Following by chromatin immunoprecipitation coupled to high-throughput DNA sequencing (ChIP-seq), we found that HrpRSL had 8, 38, and 36 targets on the genome, respectively. HrpS directly bound to the promoter regions of T3SS genes (hrpK1, hrpA2 and hopAJ1) as well as a group of non-T3SS genes (PSPPH_1496, PSPPH_1525, PSPPH_3494 and PSPPH_3495). Subsequent biochemical and genetic assays showed that HrpS independently regulated these genes in a hrpL deletion strain. In addition, a HrpS-binding motif (GTGCCAAA) in the hrpL promoter was identified by truncation, which was verified by EMSA in vitro and lux-reporter assay in vivo. On the contrary, HrpR alone couldn’t activate hrpL. Overall, our results demonstrated that HrpS directly regulated a group of T3SS and non-T3SS genes, which is independent on HrpL. HrpS functions as the center of the regulatory cascade in T3SS. This work deciphered the key HrpRSL-T3SS regulatory network, which provides insights to develop new strategies to control P. syringae infection in the future.
2018-06-30 | GSE103921 | GEO
Project description:Transcriptomic analysis of seven human peripheral blood NK cell subsets and three T cell subsets purified from healthy cytomeglovirus seropositive donors.
Epigenetic analysis including identification of open chromatin and active enhancer elements confirms key regulatory factors defining an NK cell differentiation axis.
Chromatin-immunoprecipitation sequencing reveals contribution of key transcription factors associated with NK cell differentiation including Bcl11b.
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Project description:The transcription factor GATA-1, EKLF and NF-E2 promotes erythroid differentition by regulating their target genes, however, the intricate interplays between these key TFs and microRNA genes are largely unknown. Chromatin immunoprecipitation (ChIP) of GATA-1, EKLF and NF-E2 together with microRNA genomic promoter profiling by ChIP-on-chip analysis demonstrated that GATA-1, EKLF and NF-E2 collaborately regulate a series of microRNA genes.
2011-12-31 | GSE30808 | GEO
Project description:The transcription factor GATA-1, EKLF and NF-E2 promotes erythroid differentition by regulating their target genes, however, the intricate interplays between these key TFs and microRNA genes are largely unknown. Chromatin immunoprecipitation (ChIP) of GATA-1, EKLF and NF-E2 together with microRNA genomic promoter profiling by ChIP-on-chip analysis demonstrated that GATA-1, EKLF and NF-E2 collaborately regulate a series of microRNA genes. Comparison of microRNA promoter arrays of GATA-1 VS EKLF VS NF-E2 in K562 cells suffering with hemin induced erythroid differentiation
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Project description:Objective Estrogen-related-receptor α (ERRα) plays a critical role in the transcriptional regulation of cellular bioenergetics and metabolism, and perturbations in its activity have been associated with metabolic diseases. While several coactivators and corepressors of ERRα have been identified to date, a knowledge gap remains in understanding the extent to which ERRα cooperates with coregulators in the control of gene expression. Herein, we mapped the primary chromatin-bound ERRα interactome in mouse liver. Methods RIME (Rapid Immuno-precipitation Mass spectrometry of Endogenous proteins) analysis using mouse liver samples from two circadian time points was used to catalog ERRα-interacting proteins on chromatin. The genomic crosstalk between ERRα and its identified cofactors in the transcriptional control of precise gene programs was explored through cross-examination of genome-wide binding profiles from chromatin immunoprecipitation-sequencing (ChIP-seq) studies. The dynamic interplay between ERRα and its newly uncovered cofactor Host cell factor C1 (HCFC1) was further investigated by loss-of-function studies in hepatocytes. Results Characterization of the hepatic ERRα chromatin interactome led to the identification of 48 transcriptional interactors of which 42 were previously unknown including HCFC1. Interrogation of available ChIP-seq binding profiles highlighted oxidative phosphorylation (OXPHOS) under the control of a complex regulatory network between ERRα and multiple cofactors. While ERRα and HCFC1 were found to bind to a large set of common genes, only a small fraction showed their co-localization, found predominately near the transcriptional start sites of genes particularly enriched for components of the mitochondrial respiratory chain. Knockdown studies demonstrated inverse regulatory actions of ERRα and HCFC1 on OXPHOS gene expression ultimately dictating the impact of their loss-of-function on mitochondrial respiration. Conclusions Our work unveils a repertoire of previously unknown transcriptional partners of ERRα comprised of chromatin modifiers and transcription factors thus advancing our knowledge of how ERRα regulates metabolic transcriptional programs.
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Project description:JAGGED (JAG) is a regulatory gene that controls shoot organ growth in Arabidopsis. To reveal the molecular links between JAG and the cellular activities required for tissue growth, we used chromatin immunoprecipitation-high-throughput sequencing (ChIP-Seq).
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Project description:Automated high-throughput chromatin immunoprecipitation
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Project description:We combined chromatin immunoprecipitation (ChIP) with mass spectrometry to identify key bidning partners of RPA194 (the major subunit of RNA polI) at the rDNA loci in breast cancer cells subjected to hypoxia.
2025-07-15 | PXD053040 | Pride
Project description:The Pseudomonas aeruginosa quorum-sensing (QS) systems contribute to bacterial homeostasis and pathogenicity. Although many regulators have been characterized to control the production of virulence factors and QS signaling molecules, its detailed regulatory mechanisms still remain elusive. Here, we performed chromatin immunoprecipitation followed by high-throughput DNA sequencing (ChIP-seq) on 10 key QS regulators. The direct regulation of these genes by corresponding regulator has been confirmed by Electrophoretic mobility shift assays (EMSAs) and quantitative real-time polymerase chain reactions (qRT-PCR). Binding motifs are found by using MEME suite and verified by footprint assays in vitro. Collectively, this work provides new cues to better understand the detailed regulatory networks of QS systems. ChIP-seq of 10 QS regulators in Pseudomonas aeruginosa
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Project description:R-loop remodeling dynamically regulates chromatin states and gene expression; however, its exploitation by cancer to sustain self-renewal and malignancy remains poorly understood. Here, we found that glioblastoma (GBM) stem cells (GSCs) display highly active R-loops compared to differentiated tumor progeny and neural stem cells (NSCs). Genome-wide mapping by R-loop RNA chromatin immunoprecipitation sequencing (RR-ChIP-seq) revealed cell-specific enrichment and spatial accumulation of R-loops at promoter-proximal regions in GSCs, correlating with active transcription and open chromatin states. We profiled R-loop interactomes and identified N-Acetyltransferase 10 (NAT10), an RNA N4-acetylcytidine (ac4C)-modifying enzyme, as a high-affinity R-loop-binding protein in GSCs. Driven by transcriptional activation via OLIG1, NAT10 was overexpressed in GSCs. ac4C-specific RNA immunoprecipitation sequencing (ac4C-RIP-seq) on R-loop RNA revealed genome-wide mapping of ac4C-modified R-loops with abundant ac4C-modified R-loops that regulated the genome. NAT10 catalyzed widespread ac4C deposition on the RNA stand of R-loops, stabilizing promoter-associated R-loops, and facilitating open chromatin to sustain self-renewal through core stemness regulators, including transcription factor EGR1. NAT10 knockdown suppressed proliferation and maintenance in vitro and attenuated tumor growth in vivo. Pharmacological inhibition of NAT10/ac4C-modified R-loops using the small-molecule inhibitor remodelin phenocopied NAT10 genetic targeting, demonstrating therapeutic promise for targeting cancer.
2026-04-10 | PXD077002 | Pride