Fig 2: Expansion in fmo5 (ID: Mis0185930.1) gene involved in the detoxification function of loach Misgurnus anguillicaudatus. a The growth curves of WT and fmo5 deletion (fmo5−/−) loach. b–d Histological structure analysis of intestines from WT and fmo5−/− loach. GC, goblet cell; FMH, mucosal fold height. e,f Expressions of muc2 and some endoplasmic reticulum stress (RE stress)-related genes in intestines. g Histological structures of livers from WT and fmo5−/− loach. The black dotted boxes represent the injury area. The black and white triangles represent hepatocyte (H for short). The yellow triangles represent red blood cells (RBC for short). h,i Expressions of some RE stress-related genes in livers. muc2, Mucin; atf6, Cyclic AMP-dependent transcription factor; eif2ak3, eukaryotic translation initiation factor 2-alpha kinase 3; chop, DNA damage-inducible transcript 3 protein; Gapdh, glyceraldehyde-3-phosphate dehydrogenase. Dapi, 4',6-diamidino-2-phenylindole. * significant difference (p < 0.05); ** very significant difference (p < 0.01); *** extremely significant difference (p < 0.001)

Fig 3: STING activation inhibits PLAU translation via the PERK-eIF2α signaling axis.A and B, cGAMP/diABZI repressed PLAU expression, which was abolished in STING KO MDA-MB-231 cells. MDA-MB-231 cells were treated with cGAMP/diABZI for 6 h. Cell lysates were analyzed by immunoblotting. C, cGAMP induced STING activation triggered PERK-eIF2α axis, which preceded TBK1-IRF3 signaling, as evidenced by the time course of p-eIF2α, p-TBK1, and p-IRF3. D, diABZI activated the PERK-eIF2α signaling axis in MDA-MB-231 cells, which was abolished in STING KO MDA-MB-231 cells. E, PERK inhibitors abolished STING activation-induced PLAU reduction and PERK-eIF2α axis activation, without suppressing TBK1-IRF3 axis activation in MDA-MB-231 cells.