Figure 5: GLB-12 interacts with both an intra- and extracellular superoxide dismutase.

(a) The effects of glb-12 RNAi were aggravated in a mutant for the main cytoplasmic SOD-1 and reduced in a mutant for the extracellular SOD-4 (n=3). (b,c) SOD-1 and both isoforms of SOD-4 are present in the somatic gonad, and the SOD-1 and SOD-4 reporter constructs, when expressed in the sod-1 and sod-4 mutant, respectively, were able to revert the glb-12 RNAi reduction in fecundity to WT levels (n=3). * in (c) shows significant differences for the strain carrying sod-1::mCherry compared with the sod-1 strain and for the strains carrying sod-4a/b::mCherry compared to the sod-4 strain. Scale bar: 20 μm. (d) Relative H₂O₂ levels in the somatic gonad were determined using the ratiometric probe roGFP2-ORP1. Depletion and overexpression of GLB-12 causes a decrease and increase, respectively, in intracellular H₂O₂ levels (n=6). Exposing worms to 20 mM H₂O₂ was included as a positive control (n=3). Scale bar: 10 μm. (e) Graphic showing the working model for GLB-12 signalling. (f) Introducing an intracellular and extracellular PRDX-2 mimics the effects seen for glb-12 RNAi in mutants for SOD-1 and SOD-4, respectively (n=4). (g) The anticipated effect of artificially introducing the H₂O₂ scavenger PRDX-2 on GLB-12 signalling. *P<0.05; **P<0.01 (two-sided Student t-test). Data are represented as mean±s.e.m.