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.

Highlights

  • RNA polymerase I (Pol I) transcribes the precursor for three out of the four ribosomal RNAs, which are essential components of ribosomes, required for cell growth and proliferation

  • RNA polymerase I has been identified as a potential target for cell proliferation inhibition

  • Our discovery will help to gain a better understanding of the molecular basis of ribosomal RNA synthesis and may have implications in developing strategies to control cellular growth

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Summary

Introduction

RNA polymerase I (Pol I) transcribes the precursor for three out of the four ribosomal RNAs (rRNAs), which are essential components of ribosomes, required for cell growth and proliferation. In proliferating cells of S. cerevisiae (hereafter called yeast), Pol I activity accounts for over 50% of the cellular transcriptional activity [1]. The specialized Pol I transcription machinery, including dedicated transcription factors, promotes efficient rRNA synthesis (reviewed in [2,3]). Many factors supporting Pol I transcription in vivo and in vitro have been identified in various organisms. It is still an open question how the observed high transcriptional output is mechanistically achieved

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