Abstract
Human immunodeficiency virus-1 (HIV-1) gene expression is controlled by cellular transcription factors and by virally encoded trans-activation proteins of the HIV-1 tat and art/trs genes, which are essential for viral replication1,9–11. Tat trans-activates HIV-1 gene expression by interacting with the trans-acting response element (TAR) located within the HIV-1 long terminal repeat (LTR) (ref. 2). In transient expression assays, tat mediates its effects largely by increasing the steady-state levels of messenger RNA species that contain the TAR sequence at or near their 5′ ends2–4, suggesting a function for tat either in transcription or in subsequent RNA processing. The tat gene could also facilitate translation of mRNA containing the TAR sequence5–8. To determine the mechanism of trans-activation by tat, we analysed the structure and rate of synthesis of RNA species directed by the HIV-1 LTR in transient expression assays both in the presence and absence of tat. Although the rate of HIV-1 transcription initiation was not affected by tat, transcriptional elongation beyond position +59 was seen only in the presence of tat. Thus, tat trans-activates HIV-1 transcription by relieving a specific block to transcriptional elongation within the TAR sequence.
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References
1. Chen, I. S. Y. Cell 47, 1-2 (1986). 2. Rosen, C. A., Sodroski, J. G. & Haseltine, W. A. Cell 41, 813-823 (1985). 3. Peterlin, B. M., Luciw, P. A., Barr, P. J. & Walker, M. D. Proc. natn. Acad. Sci. U.S.A. 83, 9734-9738 (1986). 4. Muesing, M. A., Smith, D. H. & Capon, D. J. Cell 48, 691-701 (1987). 5. Cullen, B. Cell 46, 973-982 (1986). 6. Wright, C. M., Felber, B. K., Paskalis, H. & Pavlakis, G. N. Science 234, 988-992 (1986). 7. Rosen, C. A. et al. Nature 319, 555-559 (1986). 8. Feinberg, M. B., Jarrett, R. F., Aldovini, A., Gallo, R. C. & Wong-Staal, F. Cell 46, 807-817 (1986). 9. Sodroski, J. G. et al. Science 229, 171-173 (1985). 10. Arya, S., Guo, C., Josephs, S. & Wong-Staal, F. Science 229, 69-73 (1985). 11. Sodroski, J. G., Patarca, R., Rosen, C. A., Wong-Staal, F. & Haseltine, W. A. Science 229, 74-77 (1985). 12. Dayton, A., Sodroski, J. G., Rosen, C. A., Goh, W. C. & Haseltine, W. A. Cell 44, 941-947 (1986). 13. Gluzman, Y. Cell 23, 175-182 (1981). 14. Mansour, S. L., Grodzicker, T. & Tjian, R. Molec. cell. Biol. 6, 2684-2694 (1986). 15. Barik, S., Ghosh, B., Whalen, W., Lazinski, D. & Das, A. Cell 50, 885-899 (1987). 16. Grayhack, E. J., Yang, Y., lau, L. F. & Roberts, J. W. Cell 42, 259-269 (1985). 17. Yanofsky, C. Nature 289, 751-758 (1981). 18. Von Hippel, P. H., Bear, D. H., Morgan, W. D. & McSwiggen, J. A. A. Rev. Biochem. 53, 389-446 (1984). 19. Platt, T. A. Rev. Biochem. 55, 339-372 (1986). 20. Dedrick, R. L., Kane, C. M. & Chamberlin, M. J. /. bioL Chem. 262, 9098-9108 (1987). 21. Reines, D., Wells, D., Chamberlin, M. J. & Kane, C. M. /. molec. Biol. 196, 299-312 (1987). 22. CnJi, G., Guise, J. W., McDevitt, M. A., Tucker, P. W. & Nevins, J. R. Genes Dev. 1, 471-481 (1987). 73. Bentley, D. L. & Groudine, M. Nature 321, 702-706 (1986). 24. Bender, T. P., Thompson, C. B. & Kuehl, W. M. Science 237, 1473-1476 (1987). 25. Rio, D. C. & Tjian, R. Cell 32, 1227-1240 (1983). 26. Lusky, M. & Botchan, M. Nature 293, 79-81 (1981). 27. Chirgwin, J. M., Przybyla, A. E., MacDonald, R. J. & Rutter, W. J. Biochemistry 18, 3294-3299 (1979). 28. Church, G. M. & Gilbert, W. Proc. natn. Acad. Sci. U.S.A. 81, 1991-1995 (1984). 29. Sanchez-Pescador, R. et al. Science 227, 484-492 (1985). 30. Queen, C. & Stafford, J. / molec. Biol. 4, 1042-1049 (1984).
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Kao, SY., Calman, A., Luciw, P. et al. Anti-termination of transcription within the long terminal repeat of HIV-1 by tat gene product. Nature 330, 489–493 (1987). https://doi.org/10.1038/330489a0
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DOI: https://doi.org/10.1038/330489a0
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