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| Status |
Public on Nov 13, 2017 |
| Title |
The Epstein-Barr virus episome maneuvers between nuclear chromatin compartments during reactivation [HiC-seq] |
| Organisms |
Homo sapiens; human gammaherpesvirus 4; human papillomavirus 31; Human gammaherpesvirus 8; Human papillomavirus 16 |
| Experiment type |
Other
|
| Summary |
Using chromatin conformation capture methods, we learned that the latent episome of the human Epstein-Barr virus (EBV) displays preferential chromosome association that correlates with gene density. The episome avoids gene-rich chromosomes and favors gene-poor chromosomes. Kaposi’s sarcoma-associated herpesvirus behaves similarly, but human papillomavirus does not, suggesting limited evolutionary conservation of this strategy. Moreover, the strongest contacts we detected between the human genome and EBV episome localized to OriP, the latent origin of replication. This genetic element, and the EBNA1 protein that binds there, are sufficient to reconstitute chromosome association preferences of the entire episome. Upon reactivation from latency, however, these preferences are lost. Detailed mapping of changes in interchromosomal contacts reveal that the episome moves away from repressive heterochromatin and toward activating euchromatin. Our work adds three-dimensional relocalization to the molecular events that occur during the genetic switch from EBV latency to reactivation. The involvement of only a myriad of interchromosomal contacts also argues for a possible role of this type of long-range association in gene regulation.
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| Overall design |
Hi-C examination of host-viral genome interactions during reactivation and latency
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| |
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| Contributor(s) |
Moquin SA, Miranda JL |
| Citation(s) |
29142137 |
| |
| Submission date |
Apr 24, 2017 |
| Last update date |
Jul 25, 2021 |
| Contact name |
JJ Miranda |
| E-mail(s) |
[email protected]
|
| Organization name |
Barnard College, Columbia University
|
| Street address |
3009 Broadway
|
| City |
New York |
| ZIP/Postal code |
10027 |
| Country |
USA |
| |
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| Platforms (6)
|
| GPL16791 |
Illumina HiSeq 2500 (Homo sapiens) |
| GPL22767 |
Illumina HiSeq 2500 (Homo sapiens; Human papillomavirus type 16) |
| GPL23185 |
Illumina HiSeq 2500 (Homo sapiens; Human gammaherpesvirus 4) |
| GPL23360 |
Illumina HiSeq 2500 (Homo sapiens; Human gammaherpesvirus 4; Human gammaherpesvirus 8) |
| GPL23361 |
Illumina HiSeq 2500 (Homo sapiens; Human papillomavirus type 31) |
| GPL23362 |
Illumina HiSeq 4000 (Homo sapiens; Human gammaherpesvirus 4) |
|
| Samples (32)
|
| GSM2587490 |
KemIII HiC rep 2 |
| GSM2587491 |
RaeI HiC rep 1 |
| GSM2587492 |
RaeI HiC rep 2 |
| GSM2587493 |
Raji HiC rep 1 |
| GSM2587494 |
Raji HiC rep 2 |
| GSM2587495 |
Namalwa HiC rep 1 |
| GSM2587496 |
Namalwa HiC rep 2 |
| GSM2587497 |
BC-1 KSHV HiC rep 1 |
| GSM2587498 |
BC-1 KSHV HiC 2 rep 2 |
| GSM2587499 |
20863 HiC rep 1 |
| GSM2587500 |
20863 HiC rep 2 |
| GSM2587501 |
9E HiC rep 1 |
| GSM2587502 |
9E HiC rep 2 |
| GSM2587503 |
K562_pD stable HiC rep 1 |
| GSM2587504 |
K562_pD stable HiC rep 2 |
| GSM2587505 |
K562_pD transient HiC |
| GSM2587506 |
K562_pDdE transient HiC |
| GSM2587508 |
RaeI shEBNA1 HiC |
| GSM2587509 |
Akata-Tet Z, LGNFR+ HiC rep 1 |
| GSM2587510 |
Akata-Tet Z, LGNFR- HiC rep 1 |
| GSM2587511 |
Akata-Tet Z, LGNFR+ HiC rep 2 |
| GSM2587512 |
Akata-Tet Z, LGNFR- HiC rep 2 |
| GSM2587513 |
Akata-Tet Z, LGNFR+ HiC rep 3 |
| GSM2587514 |
Akata-Tet Z, LGNFR- HiC rep 3 |
| GSM2587515 |
Akata-Tet Z, LGNFR+ HiC rep 4 |
| GSM2587516 |
Akata-Tet Z, LGNFR- HiC rep 4 |
| GSM2587517 |
Akata-Tet Z, LGNFR+ HiC rep 5 |
| GSM2587518 |
Akata-Tet Z, LGNFR- HiC rep 5 |
| GSM2844408 |
RaeI shCTRL HiC |
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| This SubSeries is part of SuperSeries: |
| GSE98123 |
The Epstein-Barr virus episome maneuvers between nuclear chromatin compartments during reactivation |
|
| Relations |
| BioProject |
PRJNA384032 |
| SRA |
SRP105086 |
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