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Genetic evidence indicates that the trimeric kinase CDK7—cyclin-H—Mat1 regulates cell cycle progression by phosphorylating cyclin-dependent kinases (CDKs). But the complex also functions in transcription: it is part of the basal transcription factor TFIIH, phosphorylating the RNA polymerase II C-terminal domain and nuclear receptors such as RAR
. So is the kinase a key component of the transcriptional machinery? Tomi Mäkelä and co-workers have used Cre/loxP technology to address this question by analysing the effect of loss of Mat1 in mitotic and post-mitotic cells (see p. 4275). The authors find that mitotic germ cells die rapidly once Mat1 is inactivated, presumably owing to defective CDK activation and cell cycle progression. When Mat1 is inactivated in Schwann cells (a post-mitotic cell type), however, no obvious dysfunction is evident through early adulthood, but the mutants exhibit severe hypomyelination after three months. The authors infer that these cells are able to execute a transcriptional program necessary for synthesis of myelin initially but not later on; they therefore propose that the TFIIH kinase does not play an essential role in general transcription but is instead required for synthesis of a specific subset of transcripts.
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