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P‐TEFb is not an essential elongation factor for the intronless human U2 snRNA and histone H2b genes
Author(s) -
Medlin Joanne,
Scurry Andrew,
Taylor Alice,
Zhang Fan,
Peterlin B Matija,
Murphy Shona
Publication year - 2005
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7600876
Subject(s) - biology , rna polymerase ii , p tefb , small nuclear rna , transcription factor ii d , microbiology and biotechnology , intron , rna polymerase ii holoenzyme , snrnp , cyclin dependent kinase 9 , transcription (linguistics) , gene expression , gene , genetics , rna , rna splicing , promoter , non coding rna , cyclin dependent kinase 2 , cell cycle , linguistics , philosophy
Phosphorylation of Ser2 of the heptapeptide repeat of the CTD of mammalian pol II by P‐TEFb is associated with productive elongation of transcription of protein‐coding genes. Here, we show that the CTD of pol II transcribing the human U2 snRNA genes is phosphorylated on Ser2 in vivo and that both the CDK9 kinase and cyclin T components of P‐TEFb are required for cotranscriptional recognition of the 3′ box RNA 3′ end processing signal. However, inhibitors of CDK9 do not affect transcription of the U2 genes, indicating that P‐TEFb functions exclusively as an RNA processing factor in expression of these relatively short, intronless genes. We also show that inhibition of CDK9 does not adversely affect either transcription of an intron‐less, replication‐activated histone H2b gene or recognition of the histone gene‐specific U7‐dependent RNA 3′ end formation signal. These results emphasize that the role of P‐TEFb as an activator of transcription elongation can be separated from its role in RNA processing and that neither function is universally required for expression of mammalian pol II‐dependent genes.