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ATFS-1 plays no repressive role in the regulation of epidermal immune response

Celine N Martineau1, Claire A Maynard1, Nathalie Pujol1

  • 1Aix Marseille Univ, INSERM, CNRS, CIML, Turing Centre for Living Systems, Marseille, France.

Micropublication Biology
|February 28, 2022
PubMed

Insights

Mitochondrial dysfunction suppresses antimicrobial peptide (AMP) gene induction during infection. Surprisingly, the key mitochondrial unfolded protein response (UPRmt) factor ATFS-1 is not required for this suppression.

Area of Science:

  • Cellular biology
  • Immunology
  • Mitochondrial biology

Background:

  • Fungal infection induces antimicrobial peptide (AMP) genes in the epidermis.
  • The mitochondrial unfolded protein response (UPRmt) can suppress this induction.
  • UPRmt is activated by knockdown of genes like spg-7.

Purpose of the Study:

  • To investigate the role of ATFS-1 in UPRmt-mediated suppression of AMP induction.
  • To determine if infection or wounding triggers UPRmt.

Main Methods:

  • RNA interference (RNAi) against spg-7 in an infection model.
  • Analysis of AMP gene induction.
  • Assessment of ATFS-1 requirement for UPRmt.

Main Results:

  • RNAi against spg-7 triggers UPRmt and blocks AMP induction during infection.
  • Infection alone does not trigger UPRmt.
  • ATFS-1 is not required for spg-7(RNAi)-induced suppression of AMP induction.

Conclusions:

  • Mitochondrial dysfunction suppresses the immune response during infection or wounding.
  • This suppression is independent of the key UPRmt transcription factor ATFS-1.

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