CDK9 has the intrinsic property to shuttle between nucleus and cytoplasm, and enhanced expression of cyclin T1 promotes its nuclear localization

• Published in: Journal of cellular physiology Vol. 192; no. 2; pp. 209 - 215
• Main Authors: Napolitano, Giuliana, Licciardo, Paolo, Carbone, Roberta, Majello, Barbara, Lania, Luigi
• Format: Journal Article
• Language: English
• Published: United States 01.08.2002
• Subjects: 3T3 Cells - metabolism; Active Transport, Cell Nucleus - physiology; Animals; Cell Nucleus - metabolism; Cercopithecus aethiops; COS Cells - metabolism; Cyclin T; Cyclin-Dependent Kinase 9; Cyclin-Dependent Kinases - metabolism; Cyclins - genetics; Cyclins - metabolism; Cyclins - physiology; Cytoplasm - metabolism; HeLa Cells - metabolism; Humans; Mice; Protein Transport - physiology; Subcellular Fractions - chemistry; Subcellular Fractions - enzymology
• ISSN: 0021-9541

CDK9 in association with cyclin T constitutes the P-TEFb complex that stimulates transcription elongation of RNAPII transcripts by phosphorylation of the CTD of RNAPII. Here we report subcellular distribution of P-TEFb in terms of localization of CDK9 and cyclin T1. We found that cyclin T1 is exclusively nuclear and it is present in nuclear-speckled structures. CDK9, albeit mainly nuclear, was also visualized in the cytoplasm. We determined that CDK9 is actively exported from the nucleus, and that leptomycin B (LMB), a specific inhibitor of nuclear export, inhibits this process. Interestingly, enforced expression of cyclin T1 enhances nuclear localization of CDK9. These findings reveal a novel control mechanism for the function of the P-TEFb complex.