Aspartic protease, which is part of the necrosis cell death pathway (PubMed:26795495, PubMed:12410314). Promotes B.thuringiensis Cry6Aa stability by preventing its proteolysis by host gut proteases. Required for Cry6Aa-induced necrotic death of intestinal cells (PubMed:26795495). Cry6Aa uptake into the host intestinal cells triggers an increase in intracellular Ca(2+) levels leading to lysosome rupture and to the subsequent release of asp-1 which leads to necrosis (PubMed:26795495). Interacts with B.thuringiensis endotoxin Cry6Aa; the interaction prevents Cry6Aa proteolysis by host gut proteases. Expression begins at the 2-fold embryonic stage and continues throughout the larval stages (at protein level) (PubMed:10854422). During the early stages of larval development, specifically expressed in the intestinal cells with the highest levels in the posterior intestinal cells int7 and int8 (PubMed:10854422). Not expressed in adults (PubMed:10854422). Up-regulated by B.thuringiensis endotoxin Cry6Aa (at protein level). RNAi-mediated knockdown partially prevents neuronal degeneration in a mec-4(u231), deg-1(u38) or gsa-1(Q227L) gain-of-function mutant background. Belongs to the peptidase A1 family.