Membranes can be distinguished by their lipids composition. This heterogeneity is at the center of membrane behavior allowing them to assume specifics functions. The plasma membrane is no exception as it differed from any other membrane by the presence of Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2]. My Ph.D. aims at understanding how the PI(4,5)P2 is regulated via its metabolism to orchestrates the interplay membrane-cytoskeleton. To this end my Ph.D. is structured around two compartments: the plasma membrane and its precursor, the cell plate, deprived of PI(4,5)P2 until its maturation into a functional plasma membrane. I first contributed to understand the influence of PI(4,5)P2 on plasma membrane relative events regarding notably how the PI(4,5)P2 depletion impacts the cytoskeleton organization and also how a lipid converting enzyme, SAC9, helps to restrict this lipid at the plasma membrane. Second part of my Ph.D. was center around the cytokinetic process. This process is characterized by the centrifugal expansion of a cell plate, driven by a specific cytoskeletal apparatus named the phragmoplast. At the end of cytokinesis, the growing edges of the cell plate reaches the parental plasma membrane to fuse with it, at a position defined earlier in mitosis. Here, I showed that a tight regulation of the phosphoinositides metabolism, in particular, PI(4,5)P2 exclusion from the growing phragmoplast is crucial for cell plate proper attachment. I uncover in a mutant, sac9, for which the PI(4,5)P2 is no more excluded and even enriched on the growing phragmoplast, unique double attachments of the cell plate, derived from an over-functional cytokinesis process. This failure correlates with abnormal PI(4,5)P2 accumulation at the cell plate, highlighting the critical need for phosphoinositides spatial regulation, before and during cytokinesis, to ensure a correct cell plate attachment and maturation into a plasma membrane.
Gratuit
Disciplines