TY - JOUR
T1 - Interactions between Tat and TAR and human immunodeficiency virus replication are facilitated by human cyclin T1 but not cyclins T2a or T2b
AU - Wimmer, Jörg
AU - Fujinaga, Koh
AU - Taube, Ran
AU - Cujec, Thomas P.
AU - Zhu, Yuerong
AU - Peng, Junmin
AU - Price, David H.
AU - Peterlin, B. Matija
N1 - Funding Information:
We thank Michael Armanini for his expert secretarial assistance, Mark Goldsmith and members of his laboratory for advice and expertise with viral experiments, Oliver Fackler and Satoshi Kanazawa for technical assistance and comments on the manuscript, and AIDS Reagents Suppository for reagents. This work was supported by the Howard Hughes Medical Institute and National Institutes of Health Grants AI43691 and GM 35500 (D.H.P.).
PY - 1999/3/1
Y1 - 1999/3/1
N2 - The transcriptional transactivator (Tat) from the human immunodeficiency virus (HIV) does not function efficiently in Chinese hamster ovary (CHO) cells. Only somatic cell hybrids between CHO and human cells and CHO cells containing human chromosome 12 (CHO12) support high levels of Tat transactivation. This restriction was mapped to interactions between Tat and TAR. Recently, human cyclin T1 was found to increase the binding of Tat to TAR and levels of Tat transactivation in rodent cells. By combining individually with CDK9, cyclin T1 or related cyclins T2a and T2b form distinct positive transcription elongation factor b (P-TEFb) complexes. In this report, we found that of these three cyclins, only cyclin T1 is encoded on human chromosome 12 and is responsible for its effects in CHO cells. Moreover, only human cyclin T1, not mouse cyclin T1 or human cyclins T2a or T2b, supported interactions between Tat and TAR in vitro. Finally, after introducing appropriate receptors and human cyclin T1 into CHO cells, they became permissive for infection by and replication of HIV.
AB - The transcriptional transactivator (Tat) from the human immunodeficiency virus (HIV) does not function efficiently in Chinese hamster ovary (CHO) cells. Only somatic cell hybrids between CHO and human cells and CHO cells containing human chromosome 12 (CHO12) support high levels of Tat transactivation. This restriction was mapped to interactions between Tat and TAR. Recently, human cyclin T1 was found to increase the binding of Tat to TAR and levels of Tat transactivation in rodent cells. By combining individually with CDK9, cyclin T1 or related cyclins T2a and T2b form distinct positive transcription elongation factor b (P-TEFb) complexes. In this report, we found that of these three cyclins, only cyclin T1 is encoded on human chromosome 12 and is responsible for its effects in CHO cells. Moreover, only human cyclin T1, not mouse cyclin T1 or human cyclins T2a or T2b, supported interactions between Tat and TAR in vitro. Finally, after introducing appropriate receptors and human cyclin T1 into CHO cells, they became permissive for infection by and replication of HIV.
UR - http://www.scopus.com/inward/record.url?scp=0033102387&partnerID=8YFLogxK
U2 - 10.1006/viro.1998.9589
DO - 10.1006/viro.1998.9589
M3 - Article
AN - SCOPUS:0033102387
SN - 0042-6822
VL - 255
SP - 182
EP - 189
JO - Virology
JF - Virology
IS - 1
ER -
