Model for the roles of midbody microtubules, the septins, and the ESCRT machinery in the two stages of abscission in the C. elegans embryo. Abscission occurs in two stages in wild-type C. elegans embryos. In the first stage (early abscission), cytoplasmic isolation occurs as furrow ingression completes, and an intercellular bridge forms between the two daughter cells (∼300 s). The second stage (late abscission) occurs almost one cell cycle later, coincident with the onset of anaphase of the second round of cell division. During late abscission, the intercellular bridge is remodeled, releasing fragments containing plasma membrane and cortical components (membrane shedding; 930 s), and the midbody and midbody ring are released into the posterior cell via an ESCRT-dependent process (midbody/ring release; 1,120 s). In PRC1^SPD-1-depleted embryos, events during both early and late abscission occur with normal kinetics. In septin-depleted embryos, events during both early and late abscission are defective, cytoplasmic isolation is delayed, and the midbody and midbody ring fail to release into the posterior cell. When the ESCRT machinery is depleted, the furrow envelops the midbody, and cytoplasmic isolation occurs with normal timing. However, the intercellular bridge is distended, suggesting the presence of an occlusion enveloped along with the midbody. As the intercellular bridge matures, the midbody and midbody ring are pushed to one side of the intercellular bridge and fail to release into the posterior cell.