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The human snRNA genes transcribed by RNA polymerase II (e.g. U1 and U2) have a characteristic TATA-less promoter containing an essential proximal sequence element. Formation of the 3′ end of these non-polyadenylated RNAs requires a specialized 3′ box element whose function is promoter specific. Here we show that truncation of the C-terminal domain (CTD) of RNA polymerase II and treatment of cells with CTD kinase inhibitors, including DRB (5,6-dichloro-1-β-D-ribofuranosylbenzimidazole), causes a dramatic reduction in proper 3′ end formation of U2 transcripts. Activation of 3′ box recognition by the phosphorylated CTD would be consistent with the role of phospho-CTD in mRNA processing. CTD kinase inhibitors, however, have little effect on initiation or elongation of transcription of the U2 genes, whereas elongation of transcription of the β-actin gene is severely affected. This result highlights differences in transcription of snRNA and mRNA genes.

Original publication




Journal article


EMBO Journal

Publication Date





925 - 934