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Journal of Virology, December 1998, p. 9881-9888, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Tat-Associated Kinase, TAK, Activity Is Regulated by Distinct Mechanisms in Peripheral Blood Lymphocytes and Promonocytic Cell Lines

Christine H. Herrmann,1,* Richard G. Carroll,2 Ping Wei,3,dagger Katherine A. Jones,3 and Andrew P. Rice1

Division of Molecular Virology, Baylor College of Medicine, Houston, Texas 770301; H. M. Jackson Foundation, Military HIV Research Program, Bethesda, Maryland 208892; and Regulatory Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 920373

Received 4 August 1998/Accepted 10 September 1998

TAK, a multisubunit cellular protein kinase that specifically associates with the human immunodeficiency virus Tat proteins and hyperphosphorylates the carboxyl-terminal domain of RNA polymerase II, is a cofactor for Tat and mediates its transactivation function. The catalytic subunit of TAK has been identified as cyclin-dependent kinase Cdk9, and its regulatory partner has been identified as cyclin T1; these proteins are also components of positive transcription elongation factor P-TEFb. TAK activity is up-regulated upon activation of peripheral blood lymphocytes and following macrophage differentiation of promonocytic cell lines. We have found that activation of peripheral blood lymphocytes results in increased mRNA and protein levels of both Cdk9 and cyclin T1. Cdk9 and cyclin T1 induction occurred in purified CD4+ primary T cells activated by a variety of stimuli. In contrast, phorbol ester-induced differentiation of promonocytic cell lines into macrophage-like cells produced a large induction of cyclin T1 protein expression from nearly undetectable levels, while Cdk9 protein levels remained at a constant high level. Measurements of cyclin T1 mRNA levels in a promonocytic cell line suggested that regulation of cyclin T1 occurs at a posttranscriptional level. These results suggest that cyclin T1 and TAK function may be required in differentiated monocytes and further show that TAK activity can be regulated by distinct mechanisms in different cell types.

* Corresponding author. Mailing address: Baylor College of Medicine, Division of Molecular Virology, One Baylor Plaza, Houston, TX 77030. Phone: (713) 798-6428. Fax: (713) 798-3490. E-mail: herrmann{at}bcm.tmc.edu.

dagger Present address: 15711 Mahogany Circle, Gaithersburg, MD 20878.

Journal of Virology, December 1998, p. 9881-9888, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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