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Investigating the role of the cellular RNA decay pathway during flavivirus replication

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dc.contributor.authorDenis, Denis, author
dc.contributor.authorGeiss, Brian, advisor
dc.contributor.authorWillusz, Jeffrey, committee member
dc.contributor.authorEbel, Gregory, committee member
dc.contributor.authorSnow, Christopher, committee member
dc.date.accessioned2023-01-21T01:24:10Z
dc.date.available2024-01-09T01:24:10Z
dc.date.issued2022
dc.description.abstractThe Cellular RNA decay pathway is an important regulatory system that affects both the quality and quantity of mRNA within the cells. Previous studies have shown that RNA viruses develop evasion mechanism to the cellular RNA decay pathway due to its antiviral nature. In eukaryotic cells, 5'-3' exonucleolytic decay mediated by XRN1 is known to be the major RNA decay pathway that interacts with RNA viruses. To provide RNA substrates for XRN1 degradation, cellular mRNA and viral RNA need to be processed by decapping enzymes such as DXO and DCP2 or RNA triphosphatases such as DUSP11 and NUDT2. Currently, there are few studies that have examined the roles of these proteins during RNA virus replication. In this study, we performed a loss-of-function experiment utilizing siRNA-mediated knockdown to reduce various RNA decay proteins and examine their effects on flavivirus replication. Collectively, our data suggested that knocking down DUSP11 and NUDT2 did not significantly affect the replication of infectious flaviviruses, whereas depletion of DCP2, showed significantly diminished West Nile virus and Zika virus replication but not on yellow fever virus. The results of this project indicate that DCP2 acts as a proviral factor for several but not all flaviviruses during infection and provide new insight into how flaviviruses may generate RNAs for XRN1-mediated degradation and subsequent XRN1 inhibition.
dc.format.mediumborn digital
dc.format.mediummasters theses
dc.identifierDenis_colostate_0053N_17508.pdf
dc.identifier.urihttps://hdl.handle.net/10217/235956
dc.languageEnglish
dc.language.isoeng
dc.publisherColorado State University. Libraries
dc.relation.ispartof2020-
dc.rightsCopyright and other restrictions may apply. User is responsible for compliance with all applicable laws. For information about copyright law, please see https://libguides.colostate.edu/copyright.
dc.subjectDUSP11
dc.subjectflavivirus
dc.subjectRNA decay pathway
dc.subjectDXO
dc.subjectDCP2
dc.subjectNUDT2
dc.titleInvestigating the role of the cellular RNA decay pathway during flavivirus replication
dc.typeText
dc.typeImage
dcterms.embargo.expires2024-01-09
dcterms.embargo.terms2024-01-09
dcterms.rights.dplaThis Item is protected by copyright and/or related rights (https://rightsstatements.org/vocab/InC/1.0/). You are free to use this Item in any way that is permitted by the copyright and related rights legislation that applies to your use. For other uses you need to obtain permission from the rights-holder(s).
thesis.degree.disciplineMicrobiology, Immunology, and Pathology
thesis.degree.grantorColorado State University
thesis.degree.levelMasters
thesis.degree.nameMaster of Science (M.S.)

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