Abstract
RNA polymerase I (Pol I) synthesizes ribosomal RNA (rRNA) in all eukaryotes, accounting for the major part of transcriptional activity in proliferating cells. Although basal Pol I transcription factors have been characterized in diverse organisms, the molecular basis of the robust rRNA production in vivo remains largely unknown. In S. cerevisiae, the multifunctional Net1 protein was reported to stimulate Pol I transcription. We found that the Pol I-stimulating function can be attributed to the very C-terminal region (CTR) of Net1. The CTR was required for normal cell growth and Pol I recruitment to rRNA genes in vivo and sufficient to promote Pol I transcription in vitro. Similarity with the acidic tail region of mammalian Pol I transcription factor UBF, which could partly functionally substitute for the CTR, suggests conserved roles for CTR-like domains in Pol I transcription from yeast to human.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Cell Cycle Proteins / chemistry*
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism*
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Conserved Sequence
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Humans
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Nuclear Proteins / chemistry*
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Nuclear Proteins / genetics
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Nuclear Proteins / metabolism*
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Pol1 Transcription Initiation Complex Proteins / chemistry
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Pol1 Transcription Initiation Complex Proteins / genetics
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Pol1 Transcription Initiation Complex Proteins / metabolism
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RNA Polymerase I / metabolism*
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RNA, Ribosomal / genetics
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Saccharomyces cerevisiae / genetics
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Saccharomyces cerevisiae / growth & development*
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Saccharomyces cerevisiae Proteins / chemistry*
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Saccharomyces cerevisiae Proteins / genetics
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Saccharomyces cerevisiae Proteins / metabolism*
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Sequence Deletion
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Transcription, Genetic
Substances
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Cell Cycle Proteins
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Net1 protein, S cerevisiae
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Nuclear Proteins
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Pol1 Transcription Initiation Complex Proteins
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RNA, Ribosomal
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Saccharomyces cerevisiae Proteins
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transcription factor UBF
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RNA Polymerase I
Grants and funding
This work was financed by the Deutsche Forschungsgemeinschaft (DFG) by grants to J.G., H.T., P.M., and W.S. within the collaborative research center SFB960. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.