NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE138937 Query DataSets for GSE138937
Status Public on Oct 24, 2019
Title Effect of CTCF and Rad21 knockdown on SLK cells and KSHV gene expression
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary 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.
 
Overall design Three different treatments were applied to cells: control KD, CTCF KD and Rad21 KD. Each treatment was done in triplicate.
 
Contributor(s) Swaminathan S
Citation(s) 31666380
Submission date Oct 16, 2019
Last update date Aug 06, 2020
Contact name Chris Stubben
Organization name Huntsman Cancer Institute
Department University of Utah
Street address 2000 Cir of Hope Dr
City Salt Lake City
State/province Utah
ZIP/Postal code 84103
Country USA
 
Platforms (1)
GPL16791 Illumina HiSeq 2500 (Homo sapiens)
Samples (9)
GSM4123898 12323X1 Control si KD
GSM4123899 12323X2 Control si KD
GSM4123900 12323X3 Control si KD
Relations
BioProject PRJNA577854
SRA SRP225887

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE138937_counts_raw.txt.gz 393.3 Kb (ftp)(http) TXT
SRA Run SelectorHelp
Raw data are available in SRA
Processed data are available on Series record

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap