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Measurement of mRNA Decay Rates in Saccharomyces cerevisiae Using rpb1-1 Strains
12:21

Measurement of mRNA Decay Rates in Saccharomyces cerevisiae Using rpb1-1 Strains

Published on: December 13, 2014

Loss of translational control in yeast compromised for the major mRNA decay pathway

L E A Holmes1, S G Campbell, S K De Long

  • 1Department of Biomolecular Sciences, University of Manchester Institute of Science and Technology, Manchester M60 1QD, United Kingdom.

Molecular and Cellular Biology
|March 17, 2004
PubMed

Insights

Yeast mutants with impaired mRNA decay cannot halt translation during stress. This suggests mRNA decay is crucial for regulating protein synthesis and stress adaptation in eukaryotes.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • mRNA decay and translation initiation are linked pathways controlling cytoplasmic mRNA fate.
  • The eIF2alpha kinase pathway is a conserved stress response in eukaryotes, often studied via amino acid starvation in yeast.

Purpose of the Study:

  • To investigate the role of mRNA decay in the stress response.
  • To determine if defects in mRNA decay affect global translation initiation under stress.

Main Methods:

  • Utilized yeast strains with defects in mRNA decay pathways downstream of deadenylation.
  • Analyzed global translation initiation, eIF2alpha phosphorylation, and GCN4 mRNA translation in response to stress.

Main Results:

  • Yeast strains with compromised mRNA decay failed to inhibit global translation initiation during stress.
  • These mutants displayed hallmarks of amino acid starvation, including increased eIF2alpha phosphorylation and GCN4 translation, despite maintaining high general translation.
  • Mutants appeared unresponsive to reduced ternary complex levels, suggesting enhanced mRNA recruitment.

Conclusions:

  • mRNA decay pathway integrity is essential for inhibiting global translation initiation under stress.
  • Defects in mRNA decay can decouple stress sensing from translational control, leading to aberrant stress responses.
  • Higher rates of mRNA recruitment to the 40S ribosomal subunit may explain the translational obliviousness in these mutants.

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