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Actomyosin contractility regulators stabilize the cytoplasmic bridge between the two primordial germ cells during Caenorhabditis elegans embryogenesis.

Goupil E, Amini R, Hall DH, Labbé JC

Institute of Research in Immunology and Cancer and eugenie.goupil@umontreal.ca jc.labbe@umontreal.ca.

Stable cytoplasmic bridges arise from failed cytokinesis, the last step of cell division, and are a key feature of syncytial architectures in the germline of most metazoans. Whereas the Caenorhabditiselegans germline is syncytial, its formation remains poorly understood. We found that the germline precursor blastomere, P4 , fails cytokinesis, leaving a stable cytoplasmic bridge between the two daughter cells, Z2 and Z3 Depletion of several regulators of actomyosin contractility resulted in a regression of the membrane partition between Z2 and Z3, indicating that they are required to stabilize the cytoplasmic bridge. Epistatic analysis revealed a pathway in which Rho regulators promote accumulation of the noncannonical anillin ANI-2 at the stable cytoplasmic bridge, which in turns promotes the accumulation of the nonmuscle 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 germline formation and define a set of conserved regulators that are enriched at the primordial germ cell cytoplasmic bridge to ensure its stability during embryonic development.

Mol. Biol. Cell 2017;28(26):3789-3800.

Pubmed ID: 29074566

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