Abstract
Protein kinase CK2 regulates RNA polymerase III transcription of human U6 small nuclear RNA (snRNA) genes both negatively and positively depending upon whether the general transcription machinery or RNA polymerase III is preferentially phosphorylated. Human U1 snRNA genes share similar promoter architectures as that of U6 genes but are transcribed by RNA polymerase II. Herein, we report that CK2 inhibits U1 snRNA gene transcription by RNA polymerase II. Decreased levels of endogenous CK2 correlates with increased U1 expression, whereas CK2 associates with U1 gene promoters, indicating that it plays a direct role in U1 gene regulation. CK2 phosphorylates the general transcription factor small nuclear RNA-activating protein complex (SNAP(C)) that is required for both RNA polymerase II and III transcription, and SNAP(C) phosphorylation inhibits binding to snRNA gene promoters. However, restricted promoter access by phosphorylated SNAP(C) can be overcome by cooperative interactions with TATA-box-binding protein at a U6 promoter but not at a U1 promoter. Thus, CK2 may have the capacity to differentially regulate U1 and U6 transcription even though SNAP(C) is universally utilized for human snRNA gene transcription.
Highlights
Protein kinase CK2 regulates RNA polymerase III transcription of human U6 small nuclear RNA genes both negatively and positively depending upon whether the general transcription machinery or RNA polymerase III is preferentially phosphorylated
To test whether endogenous CK2 influences human U1 gene expression in living cells, CK2 levels were reduced by RNA interference (RNAi), and the effect on U1 small nuclear RNA (snRNA) production was monitored by reverse transcription (RT)-PCR (Fig. 1B)
The proximal sequence element (PSE) is common to all human snRNA genes regardless of polymerase specificity, and the basal transcription factor small nuclear RNA-activating protein complex (SNAPC) that binds this element is used for transcription by RNA polymerases II and III [27,28,29,30,31]
Summary
Protein kinase CK2 regulates RNA polymerase III transcription of human U6 small nuclear RNA (snRNA) genes both negatively and positively depending upon whether the general transcription machinery or RNA polymerase III is preferentially phosphorylated. CK2 inhibitors interfere with Brf11⁄7TFIIIB binding to the TFIIIC complex [12], which itself recognizes intragenic promoter elements of 5 S rRNA and tRNA genes, suggesting that CK2 has a stimulatory role in RNA polymerase III transcription through enhanced preinitiation complex assembly. Consistent with this positive role, CK2 can activate RNA polymerase III transcription in human cells [12] and in this process may phosphorylate RNA polymerase III itself [13]. Oct-1 activates snRNA transcription by direct protein contacts [22,23,24] with the basal transcription factor called the snRNA-activating protein complex (SNAPC) [25], which is referred to as the proximal sequence element transcription
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