Midbody
- Tricellular junction proteins promote disentanglement of daughter and neighbour cells during epithelial cytokinesis
Highlighted Article: Daughter-neighbour cell disentanglement during multicellular cytokinesis is driven by the coordinated basal descent of the midbody and de novo assembly of tricellular septate junctions.
- Citron kinase-dependent F-actin maintenance at midbody secondary ingression sites mediates abscission
Highlighted Article: Citron kinase is required to maintain F-actin at midbody secondary ingression sites, which is necessary to prepare abscission sites for the final cut.
- FYCO1 regulates accumulation of post-mitotic midbodies by mediating LC3-dependent midbody degradation
Highlighted Article: The degradation of post-mitotic midbodies is regulated by FYCO1. Without FYCO1, midbodies accumulate, allowing for changes in cell function.
- PRL-3 disrupts epithelial architecture by altering the post-mitotic midbody position
Summary: The cancer-promoting phosphatase PRL-3 triggers ectopic lumen formation through midbody mispositioning by accelerating cytokinesis, suggesting a new oncogenic mechanism.
- C. elegans midbodies are released, phagocytosed and undergo LC3-dependent degradation independent of macroautophagy
Summary: Autophagy proteins are required for the degradation of midbodies. In C. elegans, Atg8/LC3-family proteins act during phagosome maturation rather than during macroautophagy.
- TRIM17 contributes to autophagy of midbodies while actively sparing other targets from degradation
Highlighted Article: TRIM17 regulates selective autophagy by inhibiting the degradation of a range of substrates but promoting the autophagic removal of midbodies. Thus TRIM17 facilitates the precise discrimination between potential autophagy substrates.