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EBV iPOND in cancer-causing Epstein-Barr virus infected cells

ABSTRACT: We describe how the cancer-causing Epstein-Barr virus (EBV), a prototypic herpesvirus, alters proteome at viral replication forks prominently identifies chromatin modifying and transcriptional repression proteins. Specifically, to transition from transcription, the viral DNA polymerase processivity factor EA-D is SUMOylated by the transcriptional corepressor KAP1-TRIM28. KAP1 function is triggered by phosphorylation via the PI3K-related kinase ATM and the helicase RECQ5 at the transcription machinery. SUMO-EA-D recruits the histone loader CAF1 and the methyltransferase SETDB1 to silence the parental genome, prioritizing replication. Thus, DNA repair, epigenetic, and transcription-replication interference pathways orchestrate the handover from transcription to replication, a fundamental feature of DNA viruses

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Sumita Bhaduri-McIntosh

PROVIDER: MSV000091375 | MassIVE | Mon Feb 27 17:07:00 GMT 2023

REPOSITORIES: MassIVE

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