Show simple item record

dc.contributor.advisorSugden, Bill
dc.contributor.authorKirschstein, Elijah
dc.date.accessioned2024-02-22T17:33:46Z
dc.date.available2024-02-22T17:33:46Z
dc.date.issued2023
dc.identifier.urihttp://digital.library.wisc.edu/1793/84964
dc.description.abstractWe have uncovered how Epstein-Barr virus (EBV) induces the reorganization of cellular chromatin (ROCC), where host chromatin is compacted and marginated within the nucleus. We tested the role of EBV lytic DNA amplification in driving ROCC and learned that inhibiting it supports chromatin compaction but blocks margination. We favor two steps for EBV’s ROCC: EBV first mediates a cellular response leading to global chromatin compaction, and second, viral DNA synthesis drives margination of cellular DNA. We asked if the histone-associated simian virus 40 (SV40) DNA synthesis could substitute for EBV’s histone-free viral DNA synthesis and found that EBV’s ROCC is incompatible with SV40 DNA replication. We conclude that, during its lytic phase, EBV blocks DNA synthesis in which histones are loaded onto newly synthesized DNA, in favor of its own histone-free lytic DNA amplification.en_US
dc.language.isoenen_US
dc.rightsThe author hereby grants to University of Wisconsin-Madison the permission to reproduce and to distribute publicly paper and electronic copies of this thesis document in whole or in part in any medium now known or hereafter created.en_US
dc.titleDetermining the requirement for viral DNA amplification in mediating the reorganization of cellular chromatin during the Epstein-Barr virus lytic cycleen_US
dc.typeThesisen_US


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record