KSHV's Molecular Heist: Decay of Host mRNA, PABPC Relocation, and CRM1-Mediated Liberation of Escapees

Presenter

Tarah Isabel Gervais

Campus

UMass Amherst

Sponsor

Mandy Muller, Department of Microbiology, UMass Amherst

Schedule

Session 4, 2:30 PM - 3:15 PM [Schedule by Time][Poster Grid for Time/Location]

Location

Poster Board A31, Campus Center Auditorium, Row 2 (A21-A40) [Poster Location Map]

Abstract

Kaposi's Sarcoma Associated Herpes Virus (KSHV) hijacks cellular host machinery through its viral endonuclease, SOX. SOX is responsible for degrading host mRNAs in the cytoplasm. Through this degradation of host mRNA, SOX is able to drive the relocalization from the cytoplasm to the nucleus of Polyadenylate-binding protein cytoplasmic (PABPC), a key protein that regulates the process of translation. This PABPC relocalization leads to an intriguing side effect: nuclear transcripts are now hyperadenylated, leading to the creation of a nuclear export blockade of nascent transcripts. However, a subset of host transcripts are able to actively escape this blockade and then further survive SOX activity in the cytoplasm and eventually be translated into proteins. We hypothesize that exportin 1 (XPO1), otherwise known as Chromosome Region Maintenance 1 (CRM1), acts as an alternative nuclear export for these select escaping transcripts. In order to export transcripts, CRM1 interacts with RAN-GTP. Therefore, we designed CRM1 mutants targeting CRIME and the Acidic Loop domains, as both are involved in RAN-GTP binding. These mutants will be used to assess how CRM1 regulates the export of the KSHV-resistant mRNA.

Keywords

RNA Decay, Hyperadenylation, Viral, Molecular Cloning

Research Area

Biological Organisms

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