Figure 1 ATFS-1 is not required for the induction of the epidermal immune response, nor for its inhibition:(A-D) Quantification of relative green fluorescence (GFP/size) in young adult worms after infection (orange) or not (blue) with the fungus Drechmeria coniospora treated with the either
sta-1 (control) or
spg-7 RNAi clones, with mean and SEM, **** p<0.0001. The induction of immune response was followed with a
nlp-29p::GFP reporter using the frIs7 transgene (A,C & D). The induction of UPRmt was followed with a
hsp-6p::GFP reporter using the zcIs13 transgene (B). (A-B) Compared to
sta-1 control clone, the inactivation of
spg-7 induces the UPRmt (B) and blocks the induction of
nlp-29p::GFP upon infection in the wild type (A), as previously shown (Zugasti et al., 2014). (C-D) The same results were obtained in
atfs-1(
gk3094) mutant background (C) or in the background of an
atfs-1(
tm4525) mutant rescued with a form of ATFS-1 engineered to include a strong MTS signal (bcSi81[
atfs-1(NcATP9MTS)]) (Rolland et al., 2019) (D). (E) Representatives images of the induction of immune response upon wounding followed with the same frIs7 reporter transgene. The induction of
nlp-29p::GFP reporter is visualised simultanously with the constitutive expression of
col-12p::RFP reporter in the epidermis with a GFP long pass filter. (F) Quantification of relative green fluorescence (GFP/size) in young adult worms after wounding (orange) or not (blue) treated with the either
sta-1 (control) or
spg-7 RNAi clones, with mean and SEM, **** p<0.0001.