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    ARID3B: A novel regulator of the Kaposi's sarcoma-associated herpesvirus lytic cycle

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    journal_of_virology_2016.pdf (3.115Mb)
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    Publication date
    2016-08-10
    Author
    Wood, J.J.
    Boyne, James R.
    Paulus, C.
    Jackson, B.R.
    Nevels, M.M.
    Whitehouse, A.
    Hughes, D.J.
    Keyword
    KSHV, Kaposi's sarcoma-associated hepresvirus; Primary effusion lymphoma; PEL, Kaposi's sarcoma; KS; viral gene expression; Lytic reactivation
    Rights
    2016 Wood et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license (http://creativecommons.org/licenses/by/4.0/).
    Peer-Reviewed
    Yes
    
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    Abstract
    KSHV is the causative agent of commonly fatal malignancies of immuno-compromised individuals, including primary effusion lymphoma (PEL) and Kaposi's sarcoma (KS). A hallmark of all herpesviruses is their biphasic lifecycle – viral latency and the productive lytic cycle, and it is well established that reactivation of the KSHV lytic cycle is associated with KS pathogenesis. Therefore, a thorough appreciation of the mechanisms that govern reactivation is required to better understand disease progression. The viral protein, replication and transcription activator (RTA), is the KSHV lytic switch protein due to its ability to drive the expression of various lytic genes, leading to reactivation of the entire lytic cycle. While the mechanisms for activating lytic gene expression have received much attention, how RTA impacts on cellular function is less well understood. To address this, we developed a cell line with doxycycline-inducible RTA expression and applied SILAC-based quantitative proteomics. Using this methodology, we have identified a novel cellular protein (AT-rich interacting domain containing 3B, ARID3B) whose expression was enhanced by RTA and that relocalised to replication compartments upon lytic reactivation. We also show that siRNA knockdown or overexpression of ARID3B led to an enhancement or inhibition of lytic reactivation, respectively. Furthermore, DNA affinity and chromatin immunoprecipitation assays demonstrated that ARID3B specifically interacts with A/T-rich elements in the KSHV origin of lytic replication (oriLyt), and this was dependent on lytic cycle reactivation. Therefore, we have identified a novel cellular protein whose expression is enhanced by KSHV RTA with the ability to inhibit KSHV reactivation.
    URI
    http://hdl.handle.net/10454/8805
    Version
    Accepted Manuscript
    Citation
    Wood JJ, Boyne JR, Paulus C, Jackson BR et al (2016) ARID3B: A novel regulator of the Kaposi’s sarcoma-associated herpesvirus lytic cycle. Journal of Virology. 90(20): 9543–9555.
    Link to publisher’s version
    http://dx.doi.org/10.1128/JVI.03262-15
    Type
    Article
    Collections
    Life Sciences Publications

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