Genome-wide translational changes induced by the prion [PSI+]

  • Cell Rep. 2014 Jul 24;8(2):439-48. doi: 10.1016/j.celrep.2014.06.036.
Agnès Baudin-Baillieu  1 ,  Rachel Legendre  1 ,  Claire Kuchly  1 ,  Isabelle Hatin  1 ,  Stéphane Demais  1 ,  Claire Mestdagh  1 ,  Daniel Gautheret  1 ,  Olivier Namy  2
Affiliations
  • 1. IGM, University of Paris-Sud, 91405 Orsay, France; CNRS, UMR 8621, 91405 Orsay, France.
  • 2. IGM, University of Paris-Sud, 91405 Orsay, France; CNRS, UMR 8621, 91405 Orsay, France. Electronic address: [email protected].
PMID: 25043188 DOI: 10.1016/j.celrep.2014.06.036
Abstract

Prions are infectious proteins that can adopt a structural conformation that is then propagated among Other molecules of the same protein. [PSI(+)] is an aggregated conformation of the translational release factor eRF3. [PSI(+)] modifies cellular fitness, inducing various phenotypes depending on genetic background. However, the genes displaying [PSI(+)]-controlled expression remain unknown. We used ribosome profiling in isogenic [PSI(+)] and [psi(-)] strains to identify the changes induced by [PSI(+)]. We found 100 genes with stop codon readthrough events and showed that many stress-response genes were repressed in the presence of [PSI(+)]. Surprisingly, [PSI(+)] was also found to affect reading frame selection independently of its effect on translation termination efficiency. These results indicate that [PSI(+)] has a broader impact than initially anticipated, providing explanations for the phenotypic differences between [psi(-)] and [PSI(+)] strains.