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

Fungal infection triggers the induction of antimicrobial peptide (AMP) genes in the epidermis (Pujol et al, 2008). We previously showed that this effect is suppressed by the mitochondrial unfolded protein response (UPR), which can be activated by knockdown of select genes including the mitochondrial metalloprotease (Zugasti et al, 2016). Here, we confirm that RNAi against triggers the UPR and blocks AMP induction during infection, whereas infection itself does not trigger the UPR. ATFS-1 is a key factor in the UPR, mediating much of the associated transcriptional response. We find that, surprisingly, ATFS-1 is not required for the suppression of AMP induction provoked by . These data show that the mitochondrial dysfunction that blocks the immune response upon infection or wounding is independent of ATFS-1.