The yeast mitochondrial porin represses Snf1/AMP kinase signaling to attenuate viral replication

Sabrina Chau1, Serena Marek1, Aayushee Khanna2

  • 1Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada.

Genetics
|April 24, 2026
PubMed

Insights

Fungal cells possess a novel antiviral defense mechanism. The mitochondrial Por1 protein limits RNA mycovirus replication by regulating Snf1 kinase activity, controlling nutrient availability.

Area of Science:

  • Mycology
  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Fungi are frequently infected by mycoviruses, yet the cellular antiviral mechanisms remain poorly understood.
  • Understanding how fungi combat viral infections is crucial for both basic science and potential biotechnological applications.

Purpose of the Study:

  • To identify and characterize novel antiviral defense mechanisms in the yeast Saccharomyces cerevisiae.
  • To elucidate the role of mitochondrial signaling in controlling RNA mycovirus replication.

Main Methods:

  • Investigated the role of the mitochondrial voltage-dependent anion channel (Por1) in regulating L-A RNA mycovirus replication.
  • Utilized genetic analysis, including gene deletion studies (por1Δ, snf1Δ), to explore regulatory pathways.
  • Examined the activation state of AMP-activated kinase homolog Snf1 and its signaling targets.

Main Results:

  • Discovered that Por1 prevents L-A mycovirus hyper-replication in stationary phase yeast.
  • Identified an epistatic relationship between Por1 and Snf1, indicating Por1 negatively regulates Snf1 activity.
  • Demonstrated that the Por1-Snf1 pathway limits amino acid availability, thereby restricting viral replication.

Conclusions:

  • A novel mitochondrially controlled signaling pathway involving Por1 and Snf1 acts as a physiological control mechanism against viral replication in yeast.
  • This mechanism limits viral propagation by modulating nutrient availability during stationary phase.
  • The findings reveal a new layer of eukaryotic antiviral defense.

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