Effect of CTCF and Rad21 knockdown on SLK cells and KSHV gene expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577854 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10291946.fastq.gz | Fastqsanger.gz | |||
| SRR10291947.fastq.gz | Fastqsanger.gz | |||
| SRR10291948.fastq.gz | Fastqsanger.gz | |||
| SRR10291949.fastq.gz | Fastqsanger.gz | |||
| SRR10291950.fastq.gz | Fastqsanger.gz |
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Project description:CTCF and the cohesin complex modify chromatin by binding to DNA and interacting with each other and with other cellular proteins. Both proteins regulate transcription by a variety of local effects on transcription and by long range topological effects. CTCF and cohesin also bind to herpesvirus genomes at specific sites and regulate viral transcription during latent and lytic cycles of replication. Kaposi’s sarcoma-associated herpesvirus (KSHV) transcription is regulated by CTCF and cohesin, with both proteins previously reported to act as restrictive factors for lytic cycle transcription and virion production. In this study, we examined the interdependence of CTCF and cohesin binding to the KSHV genome. ChIP-seq analyses revealed that cohesin binding to the KSHV genome is highly CTCF dependent whereas CTCF binding does not require cohesin. Further, depletion of CTCF leads to almost complete dissociation of cohesin from sites at which they colocalize. Thus, previous studies which examined the effects of CTCF depletion actually represent concomitant depletion of both CTCF and cohesin components. Analysis of the effects of single and combined depletion indicate that CTCF primarily activates KSHV lytic transcription whereas cohesin has primarily inhibitory effects. Further, CTCF or cohesin depletion was found to have regulatory effects on cellular gene expression relevant for control of viral infection, with both proteins potentially facilitating expression of multiple genes important in the innate immune response to viruses. Thus, CTCF and cohesin have both positive and negative effects on KSHV lytic replication as well as effects on the host cell that enhance antiviral defenses.
2019-10-24 | GSE138937 | GEO
Project description:Effect of CTCF and Rad21 knockdown on cell and KSHV gene expression
| PRJNA574630 | ENA
Project description:CTCF and the cohesin complex modify chromatin by binding to DNA and interacting with each other and with other cellular proteins. Both proteins regulate transcription by a variety of local effects on transcription and by long range topological effects. CTCF and cohesin also bind to herpesvirus genomes at specific sites and regulate viral transcription during latent and lytic cycles of replication. Kaposi’s sarcoma-associated herpesvirus (KSHV) transcription is regulated by CTCF and cohesin, with both proteins previously reported to act as restrictive factors for lytic cycle transcription and virion production. In this study, we examined the interdependence of CTCF and cohesin binding to the KSHV genome. ChIP-seq analyses revealed that cohesin binding to the KSHV genome is highly CTCF dependent whereas CTCF binding does not require cohesin. Further, depletion of CTCF leads to almost complete dissociation of cohesin from sites at which they colocalize. Thus, previous studies which examined the effects of CTCF depletion actually represent concomitant depletion of both CTCF and cohesin components. Analysis of the effects of single and combined depletion indicate that CTCF primarily activates KSHV lytic transcription whereas cohesin has primarily inhibitory effects. Further, CTCF or cohesin depletion was found to have regulatory effects on cellular gene expression relevant for control of viral infection, with both proteins potentially facilitating expression of multiple genes important in the innate immune response to viruses. Thus, CTCF and cohesin have both positive and negative effects on KSHV lytic replication as well as effects on the host cell that enhance antiviral defenses.
2019-10-24 | GSE138105 | GEO
Project description:Human SLK cells were infected with wildtype (wt) and LANA knockout (KO) Kaposi's sarcoma-associated herpesvirus (KSHV), separately for 3 days. Cellular gene expression changes were identified upon the wild type and LANA KO KSHV virus infection compared to the uninfected SLK cells using the human gene expression microarray U133plus2.0. 2 independent biological replicates from uninfected SLK cells, wild type KSHV infected SLK cells at 72hrs post-infection (hpi) , and LANA KO infected SLK cells at 72 hrs post-infection were collected and RNA was prepared for microarray analysis.
2016-08-01 | E-GEOD-78282 | biostudies-arrayexpress
Project description:[original title] Mock or latently infected KSHV cells (BCBL, SLK and HFF) vs common reference (mixture of RNA from both infected and uninfected cells). Expression profiling of latently infected cells using a custom tiling microarray. SLK and HFF cells were infected and selected for rKSHV.219. Mock infected SLK and HFF cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. Biological replicates were harvested and analyzed.
2010-03-24 | GSE20443 | GEO
Project description:[original title] Mock or latently infected KSHV cells (BCBL, SLK and HFF) vs common reference (mixture of RNA from both infected and uninfected cells). Expression profiling of latently infected cells using a custom tiling microarray. SLK and HFF cells were infected and selected for rKSHV.219. Mock infected SLK and HFF cells served as controls for each of these two stably infected cells, respectively. BJAB cells served as uninfected controls for the BCBL-1 cells. Biological replicates were harvested and analyzed. Two condition experiment: mock infected vs. latently infected cells. Three cell types.
2010-06-05 | E-GEOD-20443 | biostudies-arrayexpress
Project description:Human SLK cells were infected with wildtype (wt) and LANA knockout (KO) Kaposi's sarcoma-associated herpesvirus (KSHV), separately for 3 days. Cellular gene expression changes were identified upon the wild type and LANA KO KSHV virus infection compared to the uninfected SLK cells using the human gene expression microarray U133plus2.0.
2016-08-01 | GSE78282 | GEO
Project description:Total RNA was extracted from SLK cells that constitutively express select KSHV circular RNAs, and transcriptome analysis was performed by deep-sequencing (PE150).
2021-06-30 | GSE165528 | GEO
Project description:Chromatin-organizing factors, like CTCF and cohesins, have been implicated in the control of complex viral regulatory programs. We investigated the role of CTCF and cohesin in the control of the latent to lytic switch for Kaposi's Sarcoma-Associated Herpesvirus (KSHV). We found that cohesin subunits, but not CTCF, were required for the repression of KSHV immediate early gene transcription. Depletion of cohesin subunits Rad21, SMC1, or SMC3 resulted in lytic cycle gene transcription and viral DNA replication. In contrast, depletion of CTCF failed to induce lytic transcription or DNA replication. ChiP-Seq analysis revealed that cohesins and CTCF bound to several sites within the immediate early control regions for ORF50 and more distal 5' sites that also regulate the divergently transcribed ORF45-46-47 gene cluster. Rad21 depletion led to a robust increase in ORF45 and ORF47 transcripts, with similar kinetics to that observed with chemical induction by sodium butyrate. During latency, the chromatin between the ORF45 and ORF50 transcription start sites was enriched in histone H3K4me3 with elevated H3K9ac at the ORF45 promoter and elevated H3K27me3 at the ORF50 promoter. A paused form of RNA pol II was loosely associated with the ORF45 promoter region during latency, but was converted to an active elongating form upon reactivation induced by Rad21 depletion. Butyrate-induced transcription of ORF45 and ORF47 was resistant to cyclohexamide, suggesting that these genes have immediate early features similar to ORF50. Butyrate-treatment caused the rapid dissociation of cohesins and loss of CTCF binding at the immediate early gene locus, suggesting that cohesins may be a direct target of butyrate-mediated lytic induction. Our findings implicate cohesins as a major repressor of KSHV lytic gene activation, and function coordinately with CTCF to regulate the switch between latent and lytic gene activity. Study of chromatin-organizing factors, like CTCF and cohesins.
2012-06-02 | E-GEOD-38411 | biostudies-arrayexpress
Project description:Genome-wide ChIP data of CTCF and Rad21 binding in Rag1M-bM-^HM-^R/M-bM-^HM-^R pro-B cells CTCF and Rad21 binding in Rag1M-bM-^HM-^R/M-bM-^HM-^R pro-B
2011-06-07 | E-GEOD-26257 | biostudies-arrayexpress