Journal
RETROVIROLOGY
Volume 9, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1742-4690-9-53
Keywords
MOV10; Retrovirus; Retrotransposon; APOBEC3
Categories
Funding
- Department of Health via a National Institute for Health Research comprehensive Biomedical Research Centre
- St. Thomas' NHS Foundation Trust
- King's College London
- King's College Hospital NHS Foundation Trust
- U.K. Medical Research Council
- National Institutes of Health [AI070072]
- Research Councils U.K.
- European Molecular Biology Organization [ALTF 176-2007]
- Medical Research Council [G0401570, G1001081, G1000196] Funding Source: researchfish
- MRC [G1000196, G0401570, G1001081] Funding Source: UKRI
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Background: The identification of cellular factors that regulate the replication of exogenous viruses and endogenous mobile elements provides fundamental understanding of host-pathogen relationships. MOV10 is a superfamily 1 putative RNA helicase that controls the replication of several RNA viruses and whose homologs are necessary for the repression of endogenous mobile elements. Here, we employ both ectopic expression and gene knockdown approaches to analyse the role of human MOV10 in the replication of a panel of exogenous retroviruses and endogenous retroelements. Results: MOV10 overexpression substantially decreased the production of infectious retrovirus particles, as well the propagation of LTR and non-LTR endogenous retroelements. Most significantly, RNAi-mediated silencing of endogenous MOV10 enhanced the replication of both LTR and non-LTR endogenous retroelements, but not the production of infectious retrovirus particles demonstrating that natural levels of MOV10 suppress retrotransposition, but have no impact on infection by exogenous retroviruses. Furthermore, functional studies showed that MOV10 is not necessary for miRNA or siRNA-mediated mRNA silencing. Conclusions: We have identified novel specificity for human MOV10 in the control of retroelement replication and hypothesise that MOV10 may be a component of a cellular pathway or process that selectively regulates the replication of endogenous retroelements in somatic cells.
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