PI(3,4)P2-mediated cytokinetic abscission prevents early senescence and cataract formation
Federico Gulluni, Lorenzo Prever, Huayi Li, Petra Krafčíková, Ilaria Corrado, Wen‐Ting Lo, Jean Piero Margaria, Anlu Chen, Maria Chiara De Santis, Sophie Cnudde, Joseph Fogerty, Alex Yuan, Alberto Massarotti, Nasrin Torabi Sarijalo, Oscar Vadas, Roger Williams, Marcus Thelen, D.R. Powell, Markus Schueler, Michael S. Wiesener, Tamás Balla, Hagit Baris, Dov Tiosano, Brian M. McDermott, Brian D. Perkins, Alessandra Ghigo, Miriam Martini, Volker Haucke, Evžen Bouřa, Giorgio R. Merlo, David A. Buchner, Emilio Hirsch
Abstract
ESCRTing lenses away from senescence ESCRT proteins control membrane fusion in various key cellular processes, but the mechanisms involved are still incompletely understood. Gulluni et al . report that ESCRT recruitment at the cytokinetic bridge is mediated by the binding of an ESCRT-II subunit to the signaling lipid phosphatidylinositol 3,4-bisphosphate (see the Perspective by Brill and Wilde). This pathway acts in parallel to a known cascade driven by a protein called ALIX, but its failure is sufficient to lead to premature senescence in the lens of fish, mouse, and human eyes, where ALIX is expressed at lower levels. These results point to an evolutionarily conserved pathway for the cell-specific control of cytokinesis that serves to protect from senescence and the early onset of cataracts. —SMH