Supplementary Figure 7 : Pathways leading to expression of nlp-29, highlighting the newly discovered roles of HPLA and DCAR-1.

From: Activation of a G protein–coupled receptor by its endogenous ligand triggers the innate immune response of Caenorhabditis elegans

Supplementary Figure 7

Infection with D. coniospora and physical injury trigger up-regulation of the AMP nlp genes in the epidermis via the Gα protein GPA-12 that acts upstream of the PKC TPA-1, the TIR-domain adapter protein TIR-1 and a p38 MAPK cascade involving NSY-1, SEK-1 and PMK-1, as well as the STAT transcription factor-like protein STA-2. We found that the level of HPLA, which is potentially derived from tyrosine, increases upon infection. The precise site and mode of production of HPLA awaits elucidation; tyrosine is placed here at the level of the cuticle for the purpose of illustration. HPLA triggers nlp-29 gene expression via its cognate receptor DCAR-1, which is expressed at the apical surface of the epidermal syncytium hyp7. dcar-1 acts upstream of GPA-12, the p38 MAPK cassette and STA-2.