Cytokinesis is the final event in the cell division. After cytokinesis, one parent cell divided into two symmetric daughter cells. Unlike somatic cell which is symmetrically divided, oocyte meiotic maturation is highly asymmetric division, producing mature ovum and polar body. Class III phosphoinositide 3-kinase (PI3K) has been known as a key molecular component that regulates cell cycle progression, autophagy and endosomal trafficking. However, emerging evidences suggest that class III PI3K and its interactors are involved in midbody abscission during cytokinesis. Here we showed that beclin-1, a key component of PI3K is required to regulate midbody abscission during oocyte asymmetric division. Beclin-1 was widely distributed during meiotic maturation forming small vesicles. However, these vesicles were not colocalized with autophagosomal marker LC3. Instead, beclin-1 was detectable at the midbody ring during cytokinesis. Depletion of beclin-1 showed various defects including the failure of cytokinetic abscission, spindle separation and chromosome decondensation. Similar phenotype was observed when class III PI3K activity was inhibited. Therefore, our results demonstrate that PI3K is essential for cytokinesis but not autophagy during oocyte meiosis.

Arabidopsis Fused kinase TWO-IN-ONE (TIO) controls phragmoplast expansion and interacts with the Kinesin-12 subfamily proteins that anchor the plus ends of interdigitating microtubules (MTs) in the phragmoplast midzone. Previous analyses of loss-of-function mutants and RNA interference lines revealed that TIO positively controls both somatic and gametophytic cell cytokinesis, however, knowledge of the full spectrum of TIO functions during plant development remains incomplete. In order to further characterize TIO functions, we expressed TIO and a range of TIO variants under control of its own promoter in wild type Arabidopsis plants. We discovered that TIO-overexpressing transgenic lines produce enlarged pollen grains, arising from incomplete cytokinesis during male meiosis, and showed sporophytic abnormalities indicating polyploidy. These phenotypes arose independently in TIO variants that abolished either gametophytic function or the ability of TIO to interact with Kinesin-12 subfamily proteins. Interaction assays in yeast showed TIO to bind to AtNACK2/TETRASPORE and plants doubly homozygous for kinesin-12a and kinesin-12b knockout mutations to produce enlarged pollen grains. Our results show that TIO dominantly inhibits male meiotic cytokinesis in a dosage dependent manner that may involve direct binding to acomponent of the canonical NACK-PQR cytokinesis signaling pathway.