Fungal infection activates PLA2 via Toll signal pathway, which in turn induces oenocytoid lysis to release prophenoloxidase

Two entomopathogenic fungi, Beauveria bassiana (Bb) and Nomurea rileyi (Nr), infect larval of the beet armyworm, Spodoptera exigua. On the other hand, S. exigua larval exihibit both cellular and humoral immune responses against both fungal species. RNA interference (RNAi) of Toll or Imd immune signal pathways suppressed expressions of specific antimicrobial peptide genes in S. exigua. Eicosanoid is biosynthesized from arachidonic acid, which is released from phospholipid by a catalytic activity of phospholipase A2 (PLA2). Interestingly, it was proved that fungal infection activated PLA2 via Toll pathway, not via Imd pathway by specific RNAi experiments. Phenoloxidase (PO) is activated from inactive proPO, which is stored in a specific hemocyte type, oenocytoid. Oenocytoid cell lysis is induced by prostaglandins and releases proPO to plasma for its activation. This study showed that Toll RNAi also significantly inhibited oenocytoid cell lysis, presumably by shutdown of eicosanoid biosynthesis due to inactive PLA2. Taken together, fungal infection is recognized by Toll signal pathway, which activates PLA2 to induce eicosanoid biosynthesis, which results in PO activation by oenocytoid cell lysis.