Abstract
We have previously demonstrated that overexpression of Sam68 functionally substitutes for, as well as synergizes with, HIV-1 Rev in RRE-mediated gene expression and virus replication. In addition, C-terminal deletion mutants of Sam68 exhibit a transdominant negative phenotype in HIV replication. We now report that Sam68 also enhances the activities of Rev-like proteins of other complex retroviruses (e.g. HTLV-1 and EIAV) on their respective RNA targets. Furthermore, we demonstrate that Sam68 can function alone as well as synergize with Rev-MS2 and/or Rex-MS2 chimeric proteins on expression mediated by the corresponding RRE-MS2 fusion RNA element. Additionally, dominant negative mutants of Sam68 also repressed the synergistic activation of Sam68 with Rex, E-Rev, and/or Rev-MS2/Rex-MS2 on their corresponding RNA targets. Thus, Sam68 may play an important role in the post-transcriptional regulation of all complex retroviruses.
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Acknowledgements
We wish to thank Drs TJ Hope and D McDonald for Rex, XRE-CAT, ERev, ERRE-CAT, Rev(R)-MS2, DM258 and PRE-CAT expression plasmids. We also thank James Gilbert for performing the experiment on HIV-2 infection, and Jonathan Mau, Benjamin Pricer and Timothy Marsh for excellent technical support. This work was supported by NIH grants GM56089 to F Wong-Staal; AI46240 and a developmental award from the UCSD CFAR to TR Reddy.
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Reddy, T., Xu, Wd. & Wong-Staal, F. General effect of Sam68 on Rev/Rex regulated expression of complex retroviruses. Oncogene 19, 4071–4074 (2000). https://doi.org/10.1038/sj.onc.1203749
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DOI: https://doi.org/10.1038/sj.onc.1203749
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