Prion-dependent switching between respiratory competence and deficiency in the yeast nam9-1 mutant

A Chacinska1, M Boguta, J Krzewska

  • 1Institute of Biochemistry and Biophysics, 02-106 Warsaw, Poland.

Insights

The yeast prion [PSI(+)] interacts with a mutated mitochondrial protein (Nam9-1p) to cause respiratory deficiency. This interaction highlights a novel synthetic effect between cytosolic prions and mitochondrial mutations.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Nam9p is a mitochondrial ribosome protein in Saccharomyces cerevisiae.
  • A specific mutation (S82L) in Nam9p leads to respiratory deficiency and loss of mitochondrially encoded proteins like cytochrome oxidase subunit 2 (Cox2).

Purpose of the Study:

  • To investigate the cause of respiratory deficiency in the Saccharomyces cerevisiae strain MB43-nam9-1.
  • To elucidate the role of the yeast prion [PSI(+)] in the respiratory deficiency phenotype.

Main Methods:

  • Characterization of the respiration-deficient strain MB43-nam9-1.
  • Analysis of Cox2 protein levels and synthesis.
  • Investigating the effect of HSP104 manipulation, guanidine hydrochloride, and Sup35 expression.
  • Assessing the impact of introducing cytosol from [PSI(+)]-harboring yeast.

Main Results:

  • The strain MB43-nam9-1 exhibits decreased levels of some mitochondrially encoded proteins and lacks Cox2.
  • Newly synthesized Cox2 is rapidly degraded in this strain.
  • Respiratory deficiency is suppressed by HSP104 manipulation, guanidine hydrochloride, and Sup35 expression, suggesting [PSI(+)] involvement.
  • Respiratory deficiency is reinduced by transferring cytosol from [PSI(+)]-positive yeast.

Conclusions:

  • The mutation nam9-1 causes respiratory deficiency specifically in the presence of the cytosolic yeast prion [PSI(+)].
  • This study presents the first documented synthetic interaction between a cytosolic prion and a mutant mitochondrial protein.

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