| Autor: |
Connors CQ; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032., Mauro MS; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032., Wiles JT; Department of Biological Sciences, Columbia University, New York, NY 10027., Countryman AD; Department of Biomedical Engineering, Columbia University, New York, NY 10027., Martin SL; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032., Lacroix B; Université Paris Cité, CNRS, Institut Jacques Monod, F-75013 Paris, France.; Université de Montpellier, CNRS, Centre de Recherche en Biologie Cellulaire de Montpellier, UMR 5237 Montpellier, France., Shirasu-Hiza M; Department of Genetics and Development, Columbia University Irving Medical Center, New York, NY 10032., Dumont J; Université Paris Cité, CNRS, Institut Jacques Monod, F-75013 Paris, France., Kasza KE; Department of Mechanical Engineering, Columbia University, New York, NY 10027., Davies TR; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032.; Department of Biosciences, Durham University, Durham DH1 3LE, UK., Canman JC; Department of Pathology and Cell Biology, Columbia University Irving Medical Center, New York, NY 10032. |
| Abstrakt: |
Animal cell cytokinesis, or the physical division of one cell into two, is thought to be driven by constriction of an actomyosin contractile ring at the division plane. The mechanisms underlying cell type-specific differences in cytokinesis remain unknown. Germ cells are totipotent cells that pass genetic information to the next generation. Previously, using formin cyk-1 (ts) mutant Caenorhabditis elegans 4-cell embryos, we found that the P2 germ precursor cell is protected from cytokinesis failure and can divide with greatly reduced F-actin levels at the cell division plane. Here, we identified two canonical germ fate determinants required for P2-specific cytokinetic protection: PIE-1 and POS-1. Neither has been implicated previously in cytokinesis. These germ fate determinants protect P2 cytokinesis by reducing the accumulation of septin UNC-59 and anillin ANI-1 at the division plane, which here act as negative regulators of cytokinesis. These findings may provide insight into the regulation of cytokinesis in other cell types, especially in stem cells with high potency. |
