In animals, the midbody coordinates the end of cytokinesis when two daughter cells separate through abscission. Despite decades of study, whether abscission happens on one or both sides of the midbody is still under debate. Disparate models have also been proposed for the mechanisms of midbody internalization, ranging from asymmetric abscission followed by autophagy to symmetric release followed by phagocytosis. Here, we elucidate the fate of the midbody after cytokinesis in C. elegans embryos, taking advantage of their stereotyped timing and pattern of inheritance. We reveal that after symmetric abscission on both sides, the midbodies from early divisions are released outside cells. Released midbodies are internalized via CED-10/RAC1-dependent phagocytosis that further requires lipid regulators, such as the phosphatidylethanolamine flippase TAT-5 and the Class III PI3Kinase complex. We also find that the second polar body released during oocyte maturation is phagocytosed via the same pathways. Finally, we reveal that autophagy mediates degradation of the phagocytosed midbody. Based on our findings, we predict that this pathway of midbody release, phagocytosis, and degradation via autophagy is the in vivo fate of post-mitotic midbodies in animals.
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