| 180783 | Q10651 | A4_CAEEL | Amyloid-beta-like protein | DISRUPTION PHENOTYPE | Larval lethality during the L1 stage, with the formation of vacuoles in syncytial hypoderm, organ morphology defects, and molting defects (PubMed:17267616, PubMed:20862215). RNAi-mediated knockdown results in a reduced body size, transparent appearance, sluggish movement and insensitivity to touch (PubMed:18262516, PubMed:20862215). Delayed development and a molting defect that begins at the L3 to L4 larval stage transition and continues through to transition from the L4 larval stage to the young adult stage (PubMed:20862215). Increased sensitivity to acetylcholine inhibition (PubMed:20862215). Increased pharyngeal pumping (PubMed:11896189). In a let-7 mutant background, partial suppression of the let-7 bursting vulva phenotype (PubMed:28933985). Double RNAi-mediated knockdown with acn-1 in a let-7 mutant background leads to complete suppression of the heterochronic seam cell defects (PubMed:28933985). {ECO:0000269|PubMed:11896189, ECO:0000269|PubMed:17267616, ECO:0000269|PubMed:18262516, ECO:0000269|PubMed:20862215, ECO:0000269|PubMed:28933985}. |