Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA304038 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression programs depend on sequence-specific DNA binding transcription factors, but the mechanisms that control the selective binding of these factors in a chromosomal and genomic context remain enigmatic. Here, we show that two master regulators of B-cell fate, namely EBF1 and RBP-jk, show variable genome-wide chromosome distribution in two related B-lymphocyte lines carrying different forms of Epstein-Barr Virus (EBV) latency. The latency-type specific EBV-encoded EBNA2 colocalized with RBP-jk and EBF1 at induced binding sites. Colocalization of EBF1, RBP-jk, and EBNA2 correlated with transcriptional activation. Conditional expression or repression of EBNA2 lead to a rapid alteration in RBP-jk and EBF1 binding. Biochemical and shRNA depletion studies provide evidence for cooperative assembly at co-occupied sites. These findings reveal that non-DNA binding cofactors can facilitate combinatorial interactions to induce new patterns of transcription factor occupancy and gene programming Examination of EBNA2/EBF1/EBP-jk binding in MutuI and LCL cell lines
2015-12-16 | E-GEOD-75503 | biostudies-arrayexpress
Project description:Gene expression programs depend on sequence-specific DNA binding transcription factors, but the mechanisms that control the selective binding of these factors in a chromosomal and genomic context remain enigmatic. Here, we show that two master regulators of B-cell fate, namely EBF1 and RBP-jk, show variable genome-wide chromosome distribution in two related B-lymphocyte lines carrying different forms of Epstein-Barr Virus (EBV) latency. The latency-type specific EBV-encoded EBNA2 colocalized with RBP-jk and EBF1 at induced binding sites. Colocalization of EBF1, RBP-jk, and EBNA2 correlated with transcriptional activation. Conditional expression or repression of EBNA2 lead to a rapid alteration in RBP-jk and EBF1 binding. Biochemical and shRNA depletion studies provide evidence for cooperative assembly at co-occupied sites. These findings reveal that non-DNA binding cofactors can facilitate combinatorial interactions to induce new patterns of transcription factor occupancy and gene programming
2015-12-16 | GSE75503 | GEO
Project description:Gene expression programs depend on sequence-specific DNA binding transcription factors, but the mechanisms that control the selective binding of these factors in a chromosomal and genomic context remain enigmatic. Here, we show that two master regulators of B-cell fate, namely EBF1 and RBP-jk, show variable genome-wide chromosome distribution in two related B-lymphocyte lines carrying different forms of Epstein-Barr Virus (EBV) latency. The latency-type specific EBV-encoded EBNA2 colocalized with RBP-jk and EBF1 at induced binding sites. Colocalization of EBF1, RBP-jk, and EBNA2 correlated with transcriptional activation. Conditional expression or repression of EBNA2 lead to a rapid alteration in RBP-jk and EBF1 binding. Biochemical and shRNA depletion studies provide evidence for cooperative assembly at co-occupied sites. These findings reveal that non-DNA binding cofactors can facilitate combinatorial interactions to induce new patterns of transcription factor occupancy and gene programming
2015-12-16 | GSE75385 | GEO
Project description:Combinatorial Control of RBP-jk and EBF1 Chromosome Occupancy induced by viral co-activator EBNA2
| PRJNA304432 | ENA
Project description:Combinatorial Control of RBP-jk and EBF1 Chromosome Occupancy induced by viral co-activator EBNA2 [ChIP-seq]
| PRJNA304435 | ENA
Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphoma (PEL). All PEL cell lines are infected with KSHV, and 70% are co-infected with Epstein-Barr Virus (EBV). KSHV reactivation from latency requires promoter-specific transactivation by the KSHV Rta protein through interactions with RBP-Jk (CSL), the cellular DNA binding component of the Notch signal transduction pathway. EBV transformation of primary B cells requires EBV nuclear antigen (EBNA)-2 to interact with RBP-Jk to direct the latent viral and cellular gene expression program. Although KSHV Rta and EBV EBNA-2 both require RBP-Jk for transactivation, previous studies have suggested that RBP-Jk-dependent transactivators do not function identically. We have found that the EBV latent protein LMP-1 is expressed in less than 5% of KSHV+/EBV+ PEL cells, but is induced in an Rta-dependent fashion when KSHV reactivates. KSHV Rta transactivates the EBV latency promoters in an RBP-Jk-dependent fashion and forms a ternary complex with RBP-Jk on the promoters. In B cells that are conditionally transformed by EBV alone, we show that KSHV Rta complements a short-term EBNA2 growth deficiency in an autocrine/paracrine manner. Complementaton of EBNA2-deficiency by Rta depends on RBP-Jk and LMP-1, and Rta transactivation is required for optimal growth of KSHV+/EBV+ PEL lines. Our data suggest that Rta can contribute to EBV-driven cellular growth by transactivating RBP-Jk-dependent EBV latency genes. However, our data also suggest that EBNA2 and Rta induce distinct alterations in the cellular proteomes that contribute to growth of infected cells. EREB2-5 cells were transfected and grown in the presence or absence of β-estradiol, as described. Seven days post-transfection, protein extracts were prepared, and 200 ugs. of each were analyzed using the RayBio Human Apoptosis Antibody Array Kit (RayBiotech) as per manufacturers suggestions. The membranes were exposed to autoradiography film for different times to detect the chemiluminescent signals. Images with signals in linear range were quantitated using the program ImageJ [59]. For each membrane, signals from the negative control spots were averaged, and then subtracted from each of the other spots. A signal was considered valid if its value exceeded both its average local background, and the average of all valid negative control values. Valid signals were normalized using the positive control spots (for cellular BID protein). Fold change in signals for each spot were quantitated by dividing by the valid signals for each corresponding spot on the minus β-estradiol membrane. Average fold change, and standard deviation, were calculated for each protein.
2010-12-31 | E-GEOD-21375 | biostudies-arrayexpress
Project description:Kaposi’s sarcoma-associated herpesvirus (KSHV) is the etiologic agent of primary effusion lymphoma (PEL). All PEL cell lines are infected with KSHV, and 70% are co-infected with Epstein-Barr Virus (EBV). KSHV reactivation from latency requires promoter-specific transactivation by the KSHV Rta protein through interactions with RBP-Jk (CSL), the cellular DNA binding component of the Notch signal transduction pathway. EBV transformation of primary B cells requires EBV nuclear antigen (EBNA)-2 to interact with RBP-Jk to direct the latent viral and cellular gene expression program. Although KSHV Rta and EBV EBNA-2 both require RBP-Jk for transactivation, previous studies have suggested that RBP-Jk-dependent transactivators do not function identically. We have found that the EBV latent protein LMP-1 is expressed in less than 5% of KSHV+/EBV+ PEL cells, but is induced in an Rta-dependent fashion when KSHV reactivates. KSHV Rta transactivates the EBV latency promoters in an RBP-Jk-dependent fashion and forms a ternary complex with RBP-Jk on the promoters. In B cells that are conditionally transformed by EBV alone, we show that KSHV Rta complements a short-term EBNA2 growth deficiency in an autocrine/paracrine manner. Complementaton of EBNA2-deficiency by Rta depends on RBP-Jk and LMP-1, and Rta transactivation is required for optimal growth of KSHV+/EBV+ PEL lines. Our data suggest that Rta can contribute to EBV-driven cellular growth by transactivating RBP-Jk-dependent EBV latency genes. However, our data also suggest that EBNA2 and Rta induce distinct alterations in the cellular proteomes that contribute to growth of infected cells.
2010-12-31 | GSE21375 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246059 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246061 | GEO
Project description:There are two major types of Epstein-Barr Virus (EBV): type 1 (EBV-1) and type 2 (EBV-2). EBV functions by manipulating gene expression in host B cells, using virus-encoded gene regulatory proteins including Epstein Barr Nuclear Antigen 2 (EBNA2). While type 1 EBNA2 is known to interact with human transcription factors (hTFs) like RBPJ, EBF1, and SPI1, type 2 EBNA2 shares only ~50% amino acid identity and may have distinct effects on the genome. In this study, we examined EBNA2 binding in EBV-1 and EBV-2 transformed human B cells to identify shared and unique EBNA2 interactions with the human genome, revealing thousands of type-specific EBNA2 ChIP-seq peaks. Our analyses revealed that both types 1 and 2 EBNA2 strongly bind to SPI1 and AP-1 motifs (BATF and JUNB). However, type 1 EBNA2 showed preferential co-occupancy with EBF1, and type 2 EBNA2 with RBPJ. These differences in b hTF co-occupancy revealed type-specific gene expression of known EBNA2 targets. Both type 1 and 2 EBNA2 binding events were highly enriched at systemic lupus erythematosus (SLE) and showed type-specific enrichment at the risk loci of multiple sclerosis (type 1) and primary biliary cholangitis (type 2). Collectively, this study reveals extensive type-specific EBNA2 interactions with the human genome, genotype-dependent binding, and distinct associations with autoimmune disorders. Our results highlight the importance of considering EBV type in disease-related investigations.
2024-03-12 | GSE246060 | GEO