TY - JOUR
T1 - Regulation of HTLV-II gene expression by rex involves positive and negative cis-acting elements in the 5′ long terminal repeat
AU - Black, Alexander C.
AU - Chen, Irvin Sy
AU - Arrigo, Salvatore
AU - Ruland, Cristina T.
AU - Allogiamento, Thomas
AU - Chin, Eva
AU - Rosenblatt, Joseph D.
N1 - Funding Information:
We thank Patrick Green and Judy Gasson for helpful comments on the manuscript, William Wachsman for oligonucleotides, Wendy Aft for invaluable assistance in preparation of the manuscript, and Joyce Fujii and Ira Smalberg for technical assistance. This work was supported by grants from the Leukemia Society America; the California Institute for Cancer Research; National Institutes of Health GrantsCA38597,CA01314,CA53632,CA52410,CA01811,CA 32737, and CA 43370; and the Universitywide R87LA057.
PY - 1991/4
Y1 - 1991/4
N2 - Regulation of human T-cell leukemia virus type II (HTLV-II) gene expression by the trans-acting viral protein, Rex, is mediated through specific cis-acting sequences in the HTLV-II long terminal repeat (LTR). Augmentation of 5′ LTR-linked gene expression by Rex requires two distinct cis-acting elements: one termed the "Rex-responsive element" (RxRE), which allows Rex to overcome the inhibitory effect of a second, termed the "cis-acting repressive sequences" (CRS). The HTLV-II RxRE is located between nt +91 and +317 relative to the cap site in the R/U5 region of the 5′ LTR, and the HTLV-II CRS is contained within the RxRE from nt +208 to +317, which is downstream of the splice donor site, in the R/U5 region of the 5′ LTR. Deletion of the CRS results in significantly increased cytoplasmic levels of LTR-linked mRNA independent of the presence of Rex. Our results show that Rex acts post-transcriptionally and induces a shift from nucleus to cytoplasm of gag/pol mRNA, the only HTLV-II mRNA that contains both the RxRE and the CRS in the 5′ LTR-derived leader sequence.
AB - Regulation of human T-cell leukemia virus type II (HTLV-II) gene expression by the trans-acting viral protein, Rex, is mediated through specific cis-acting sequences in the HTLV-II long terminal repeat (LTR). Augmentation of 5′ LTR-linked gene expression by Rex requires two distinct cis-acting elements: one termed the "Rex-responsive element" (RxRE), which allows Rex to overcome the inhibitory effect of a second, termed the "cis-acting repressive sequences" (CRS). The HTLV-II RxRE is located between nt +91 and +317 relative to the cap site in the R/U5 region of the 5′ LTR, and the HTLV-II CRS is contained within the RxRE from nt +208 to +317, which is downstream of the splice donor site, in the R/U5 region of the 5′ LTR. Deletion of the CRS results in significantly increased cytoplasmic levels of LTR-linked mRNA independent of the presence of Rex. Our results show that Rex acts post-transcriptionally and induces a shift from nucleus to cytoplasm of gag/pol mRNA, the only HTLV-II mRNA that contains both the RxRE and the CRS in the 5′ LTR-derived leader sequence.
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U2 - 10.1016/0042-6822(91)90875-C
DO - 10.1016/0042-6822(91)90875-C
M3 - Article
C2 - 2014632
AN - SCOPUS:0025877715
VL - 181
SP - 433
EP - 444
JO - Virology
JF - Virology
SN - 0042-6822
IS - 2
ER -