| 173064 | Q9XWD6 | CED1_CAEEL | Cell death abnormality protein 1 | DISRUPTION PHENOTYPE | Accumulation of cell corpses (PubMed:26598553). Appears immunocompromised resulting in susceptibility to bacterial infection (PubMed:6857247, PubMed:1936965, PubMed:18606143). Reduced or lack of association of ppk-3 and rab-7 with the phagosomal surface (PubMed:18351800). Defective in the recruitment of lysosomes to phagosomes (PubMed:16740477). Double knockout with the P-granule component pgl-1 results in an increased number of cell corpses in the gonad as compared to the ced-1 single mutant (PubMed:26598553). Conversely, double knockout with pgl-1 or pgl-3 results in reduced somatic cell apoptosis (PubMed:27650246). Double knockout with the synthetic multivulva class B protein hpl-2 results in reduced somatic cell apoptosis at 25 degrees Celsius (PubMed:27650246). Triple knockout with hpl-2 and pgl-1 partially recovers the reduced somatic cell apoptotic cell defect in the ced-1 and hpl-2 double knockout (PubMed:27650246). Triple knockout with hpl-2 and pgl-1 and knockdown with either ced-3 or ced-4 reduces the somatic cell apoptosis defect in the ced-1, hpl-2 and pgl-1 triple knockout (PubMed:27650246). Double knockout with hpl-2 and knockdown with either pgl-1, pgl-3, glh-1 or glh-4 RNAi rescues the reduced somatic cell apoptotic cell defect in the ced-1 and hpl-2 double knockout (PubMed:27650246). Knockout with RNAi-mediated knockdown of synthetic multivulva class B proteins lin-9, lin-35, lin-37 or lin-54 results in reduced somatic cell apoptosis (PubMed:27650246). {ECO:0000269|PubMed:16740477, ECO:0000269|PubMed:18351800, ECO:0000269|PubMed:18606143, ECO:0000269|PubMed:1936965, ECO:0000269|PubMed:26598553, ECO:0000269|PubMed:27650246, ECO:0000269|PubMed:6857247}. |