Uncoupling ribosome biogenesis regulation from RNA polymerase I activity during herpes simplex virus type 1 infection

  1. Stéphane Belin1,2,
  2. Karine Kindbeiter3,
  3. Sabine Hacot1,2,
  4. Marie Alexandra Albaret1,2,3,
  5. Jean-Xavier Roca-Martinez1,2,3,
  6. Gabriel Thérizols1,2,
  7. Olivier Grosso4 and
  8. Jean-Jacques Diaz1,2
  1. 1Centre National de la Recherche Scientifique (CNRS), Université de Lyon, Lyon F-69003, France
  2. 2Centre de Génétique Moléculaire et Cellulaire, Centre Léon Bérard, Université de Lyon, Lyon F-69373, France
  3. 3Idéalp-Pharma, Villeurbanne, Cedex 69603, France
  4. 4L'Institut de Physique Nucléaire de Lyon (INPL), Université de Lyon, Villeurbanne, Cedex 69622, France

Abstract

The ribosome is the central effector of protein synthesis, and its synthesis is intimately coordinated with that of proteins. At present, the most documented way to modulate ribosome biogenesis involves control of rDNA transcription by RNA polymerase I (RNA Pol I). Here we show that after infection of human cells with herpes simplex virus type 1 (HSV-1) the rate of ribosome biogenesis is modulated independently of RNA Pol I activity by a dramatic change in the rRNA maturation pathway. This process permits control of the ribosome biogenesis rate, giving the possibility of escaping ribosomal stress and eventually allowing assembly of specialized kinds of ribosomes.

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Footnotes

  • Reprint requests to: Jean-Jacques Diaz, Centre de Génétique Moléculaire et Cellulaire, Centre Léon Bérard, Université de Lyon, Lyon F-69373, France; e-mail: diazjj{at}lyon.fnclcc.fr; fax: 33-4-72432685.

  • Article published online ahead of print Article and publication date are at http://www.rnajournal.org/cgi/doi/10.1261/rna.1935610.

    • Received September 23, 2009.
    • Accepted October 8, 2009.
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