Fig. 6: Model summarizing the role of PIPKIγ-i3/i5 during cytokinesis.
a Anillin (turquoise) and septins (green) are enriched at the cleavage furrow, where they act as scaffolds to initiate and sustain actomyosin-mediated constriction. b Through interaction with septins, PIPKIγ-i3/i5 (yellow) are recruited to the furrow, where they generate a local pool of PI(4,5)P2 (red). This pool is required for the maintenance of anillin and centralspindlin (blue) at the nascent midbody. c The centralspindlin-mediated tethering of the furrow membrane to microtubules possibly facilitates the translocation of septins onto bridge microtubules, and septin association with PRC1 (orange). d Presence of septins on bridge microtubules favors their bundling, while the ICB matures and elongates. e Depletion of PIPKIγ-i3/i5 disrupts the localized synthesis of PI(4,5)P2 at the nascent midbody, impairing centralspindlin tethering to the plasma membrane. f Mislocalized synthesis of PI(4,5)P2 may contribute to the scattering of anillin and septins. Disorganized septins (and anillin) further affect the maintenance of centralspindlin at the midbody and the maturation of the ICB. (Created with BioRender.com).
