| Literature DB >> 34882480 |
Federico Gulluni1, Lorenzo Prever1, Huayi Li1, Petra Krafcikova2, Ilaria Corrado1, Wen-Ting Lo3, Jean Piero Margaria1, Anlu Chen4, Maria Chiara De Santis1, Sophie J Cnudde1, Joseph Fogerty5, Alex Yuan5, Alberto Massarotti6, Nasrin Torabi Sarijalo7, Oscar Vadas8,9, Roger L Williams10, Marcus Thelen11, David R Powell12, Markus Schueler13, Michael S Wiesener7, Tamas Balla14, Hagit N Baris15,16,17, Dov Tiosano15,17, Brian M McDermott18,19, Brian D Perkins5, Alessandra Ghigo1, Miriam Martini1, Volker Haucke3,19, Evzen Boura2, Giorgio Roberto Merlo1, David A Buchner4,20, Emilio Hirsch1.
Abstract
Cytokinetic membrane abscission is a spatially and temporally regulated process that requires ESCRT (endosomal sorting complexes required for transport)–dependent control of membrane remodeling at the midbody, a subcellular organelle that defines the cleavage site. Alteration of ESCRT function can lead to cataract, but the underlying mechanism and its relation to cytokinesis are unclear. We found a lens-specific cytokinetic process that required PI3K-C2α (phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2α), its lipid product PI(3,4)P2 (phosphatidylinositol 3,4-bisphosphate), and the PI(3,4)P2–binding ESCRT-II subunit VPS36 (vacuolar protein-sorting-associated protein 36). Loss of each of these components led to impaired cytokinesis, triggering premature senescence in the lens of fish, mice, and humans. Thus, an evolutionarily conserved pathway underlies the cell type–specific control of cytokinesis that helps to prevent early onset cataract by protecting from senescence.Entities:
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Year: 2021 PMID： 34882480 PMCID： PMC7612254 DOI： 10.1126/science.abk0410
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 63.714