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Altered rRNA processing disrupts nuclear RNA homeostasis via competition for the poly(A)-binding protein Nab2.

Nucleic Acids Res. 2020 Nov 18;48(20):11675-11694
Lisbeth-Carolina Aguilar 1 , Biplab Paul 2 , Taylor Reiter 3 , Louis Gendron 4 , Arvind Arul Nambi Rajan 5 , Rachel Montpetit 6 , Christian Trahan 1 , Sebastian Pechmann 4 , Marlene Oeffinger 7 , Ben Montpetit 6
Lisbeth-Carolina Aguilar 1 , Biplab Paul 2 , Taylor Reiter 3 , Louis Gendron 4 , Arvind Arul Nambi Rajan 5 , Rachel Montpetit 6 , Christian Trahan 1 , Sebastian Pechmann 4 , Marlene Oeffinger 7 , Ben Montpetit 6
+ et al

[No authors listed]

Author information
  • 1 Department for Systems Biology, Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
  • 2 Department of Cell Biology, University of Alberta, Edmonton, Canada.
  • 3 Food Science Graduate Group, University of California Davis, Davis, CA, USA.
  • 4 Département de biochimie et médecine moléculaire, Université de Montréal, Montréal, QC, Canada.
  • 5 Biochemistry, Molecular, Cellular and Developmental Biology Graduate Group, University of California Davis, Davis, CA, USA.
  • 6 Department of Viticulture and Enology, University of California Davis, Davis, CA, USA.
  • 7 Division of Experimental Medicine, McGill University, Montreal, QC, Canada.

摘要

RNA-binding proteins (RBPs) are key mediators of RNA metabolism. Whereas some RBPs exhibit narrow transcript specificity, others function broadly across both coding and non-coding RNAs. Here, in Saccharomyces cerevisiae, we demonstrate that changes in RBP availability caused by disruptions to distinct cellular processes promote a common global breakdown in RNA metabolism and nuclear RNA homeostasis. Our data shows that stabilization of aberrant ribosomal RNA (rRNA) precursors in an enp1-1 mutant causes phenotypes similar to RNA exosome mutants due to nucleolar sequestration of the poly(A)-binding protein (PABP) Nab2. Decreased nuclear PABP availability is accompanied by genome-wide changes in RNA metabolism, including increased pervasive transcripts levels and snoRNA processing defects. These phenotypes are mitigated by overexpression of PABPs, inhibition of rDNA transcription, or alterations in TRAMP activity. Our results highlight the need for cells to maintain poly(A)-RNA levels in balance with PABPs and other RBPs with mutable substrate specificity across nucleoplasmic and nucleolar RNA processes.

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