Sumoylation of Rap1 mediates the recruitment of TFIID to promote transcription of ribosomal protein genes

  1. Jorrit M. Enserink1,2
  1. 1Institute of Microbiology, Clinic for Diagnostics and Intervention, Oslo University Hospital, N-0027 Oslo, Norway;
  2. 2University of Oslo, 0316 Oslo, Norway;
  3. 3The Biotechnology Centre of Oslo, University of Oslo, 0349 Oslo, Norway;
  4. 4Department of Tumor Biology, The Norwegian Radium Hospital, and Genomics Core Facility, Oslo University Hospital, NO-0310 Oslo, Norway
  1. Corresponding author: jorrit.enserink{at}rr-research.no
  1. 5 These authors contributed equally to this work.

Abstract

Transcription factors are abundant Sumo targets, yet the global distribution of Sumo along the chromatin and its physiological relevance in transcription are poorly understood. Using Saccharomyces cerevisiae, we determined the genome-wide localization of Sumo along the chromatin. We discovered that Sumo-enriched genes are almost exclusively involved in translation, such as tRNA genes and ribosomal protein genes (RPGs). Genome-wide expression analysis showed that Sumo positively regulates their transcription. We also discovered that the Sumo consensus motif at RPG promoters is identical to the DNA binding motif of the transcription factor Rap1. We demonstrate that Rap1 is a molecular target of Sumo and that sumoylation of Rap1 is important for cell viability. Furthermore, Rap1 sumoylation promotes recruitment of the basal transcription machinery, and sumoylation of Rap1 cooperates with the target of rapamycin kinase complex 1 (TORC1) pathway to promote RPG transcription. Strikingly, our data reveal that sumoylation of Rap1 functions in a homeostatic feedback loop that sustains RPG transcription during translational stress. Taken together, Sumo regulates the cellular translational capacity by promoting transcription of tRNA genes and RPGs.

Footnotes

  • [Supplemental material is available for this article.]

  • Article published online before print. Article, supplemental material, and publication date are at http://www.genome.org/cgi/doi/10.1101/gr.185793.114.

  • Freely available online through the Genome Research Open Access option

  • Received October 13, 2014.
  • Accepted March 17, 2015.

This article, published in Genome Research, is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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