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Molecular and Cellular Biology, July 2007, p. 4641-4651, Vol. 27, No. 13
0270-7306/07/$08.00+0     doi:10.1128/MCB.00857-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Regulation of P-TEFb Elongation Complex Activity by CDK9 Acetylation{triangledown}

Junjiang Fu,1 Ho-Geun Yoon,2 Jun Qin,1,3 and Jiemin Wong1*

Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030,1 Department of Biochemistry and Molecular Biology, College of Medicine, Yonsei University, 134 Sicnchon-dong, Seodaemun-gu, Seoul 120-752, South Korea,2 Department of Biochemistry, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 770303

Received 14 May 2006/ Returned for modification 21 June 2006/ Accepted 10 April 2007

P-TEFb, comprised of CDK9 and a cyclin T subunit, is a global transcriptional elongation factor important for most RNA polymerase II (pol II) transcription. P-TEFb facilitates transcription elongation in part by phosphorylating Ser2 of the heptapeptide repeat of the carboxy-terminal domain (CTD) of the largest subunit of pol II. Previous studies have shown that P-TEFb is subjected to negative regulation by forming an inactive complex with 7SK small RNA and HEXIM1. In an effort to investigate the molecular mechanism by which corepressor N-CoR mediates transcription repression, we identified HEXIM1 as an N-CoR-interacting protein. This finding led us to test whether the P-TEFb complex is regulated by acetylation. We demonstrate that CDK9 is an acetylated protein in cells and can be acetylated by p300 in vitro. Through both in vitro and in vivo assays, we identified lysine 44 of CDK9 as a major acetylation site. We present evidence that CDK9 is regulated by N-CoR and its associated HDAC3 and that acetylation of CDK9 affects its ability to phosphorylate the CTD of pol II. These results suggest that acetylation of CDK9 is an important posttranslational modification that is involved in regulating P-TEFb transcriptional elongation function.

* Corresponding author. Present address: Institute of Biomedical Sciences, College of Life Science, East China Normal University, Dongchuan Road 500, Shanghai 200241, China. Phone: 021-54344030. Fax: 021-54344922. E-mail: jmweng{at}bio.ecnu.edu.cn

{triangledown} Published ahead of print on 23 April 2007.

Molecular and Cellular Biology, July 2007, p. 4641-4651, Vol. 27, No. 13
0270-7306/07/$08.00+0     doi:10.1128/MCB.00857-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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