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Vol. 12, No. 22, pp. 3541-3550, November 15, 1998
Howard Hughes Medical Institute, Division of Nucleic Acids
Enzymology, Department of Biochemistry, Robert Wood Johnson Medical
School, University of Medicine and Dentistry of New Jersey,
Piscataway, New Jersey 08854-5635 USA
TFIIH is a multisubunit complex, containing ATPase, helicases, and
kinase activities. Functionally, TFIIH has been implicated in
transcription by RNA polymerase II (RNAPII) and in nucleotide excision
repair. A member of the cyclin-dependent kinase family, CDK7, is the
kinase subunit of TFIIH. Genetically, CDK7 homologues have been
implicated in transcription in Saccharomyces cerevisiae, and in
mitotic regulation in Schizosaccharomyces pombe. Here we show
that in mitosis the CDK7 subunit of TFIIH and the largest subunit of
RNAPII become hyperphosphorylated. MPF-induced phosphorylation of CDK7
results in inhibition of the TFIIH-associated kinase and transcription
activities. Negative and positive regulation of TFIIH requires
phosphorylation within the T-loop of CDK7. Our data establishes TFIIH
and its subunit CDK7 as a direct link between the regulation of
transcription and the cell cycle.
[Key Words: Transcription; TFIIH; CDK7; phosphorylation; cell cycle]
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