| 172856 | A0A0K3AWM6 | MOM5_CAEEL | Protein mom-5 | DISRUPTION PHENOTYPE | Embryonic lethal with severely defective embryonic morphogenesis (PubMed:9288749, PubMed:9288750, PubMed:15620652). Embryos have defective mitotic spindle orientation in the 8-cell stage ABar blastomere (PubMed:9288749, PubMed:9288750, PubMed:20126385). Furthermore, there is disrupted asymmetric distribution of the transcription factor pop-1 and the disheveled homolog dsh-2, which are required for cell fate decisions in 8-cell stage ABar blastomeres and their descendants (PubMed:12810601, PubMed:15990090). There is also abnormal distal tip cell migration along the anterior-posterior axis of the body and defective clearance of apoptotic cell corpses in embryos (PubMed:20126385, PubMed:26292279). Both double knockout with unc-5 RNAi and knockdown by RNAi in an unc-40 mutant background suppresses the migratory defect of distal tip cells in the mom-5 and unc-40 single mutants (PubMed:26292279). Double knockout with Wnt receptor cfz-2 results in enhanced CAN neuron migration defects and also rescues the ALM migration defects in the single cfz-2 knockout (PubMed:16109397). Double knockout with Wnt receptor mig-1 results in enhanced HSN neuron migration defects and also in anterior-posterior axon guidance defects of PVM and AVM touch neurons (PubMed:16516839). RNAi-mediated knockdown results in embryonic lethality, but surviving animals display morphogenesis defects and PHA phasmid neuron duplication (PubMed:15990090). {ECO:0000269|PubMed:12810601, ECO:0000269|PubMed:15620652, ECO:0000269|PubMed:15990090, ECO:0000269|PubMed:16109397, ECO:0000269|PubMed:16516839, ECO:0000269|PubMed:20126385, ECO:0000269|PubMed:26292279, ECO:0000269|PubMed:9288749, ECO:0000269|PubMed:9288750}. |