Stable cytoplasmic bridges arise from failed cytokinesis, the last step of cell division, and are a key feature of syncytial architectures in the germ line of most metazoans. Whereas the C. elegans germ line is syncytial, its formation remains poorly understood. We studied the role of ANI-2, a non-canonical and shorter form of the actomyosin scaffold protein anillin that is expressed specifically during embryogenesis in the germ line precursor blastomere, P4. We found that the P4 blastomere does not complete abscission following cytokinesis, leaving a stable cytoplasmic bridge between the two daughter cells. Interestingly, depletion of ANI-2 results in a regression of the membrane partition between the two cells, indicating that ANI-2 is required to stabilize the cytoplasmic bridge. We identified several contractility regulators that, like ANI-2, localize to the cytoplasmic bridge and are required to stabilize it. Epistatic analysis of these regulators mutual dependencies revealed a pathway in which Rho regulators promote ANI-2 accumulation at the stable cytoplasmic bridge, which in turns promotes the accumulation of the non-muscle myosin II NMY-2 and the midbody component CYK-7 at the bridge, in part by limiting the accumulation of canonical anillin ANI-1. Our results uncover key steps in C. elegans germ line formation and define a set of conserved regulators that ensure the proper stability of the primordial germ cell cytoplasmic bridge during embryonic development.