Keep it on the edge: The post-mitotic midbody as a polarity signal unit

Abstract

The maintenance of the epithelial architecture during tissue proliferation is achieved by apical positioning of the midbody after cell division. Consequently, midbody mislocalization contributes to epithelial architecture disruption, a fundamental event during epithelial tumorigenesis. Studies in 3D polarized epithelial MDCK or Caco2 cell models, where midbody misplacement leads to multiple ectopic but fully polarized lumen-containing cysts, revealed that this phenotype can be caused by 2 different scenarios: the loss of mitotic spindle orientation or the loss of asymmetric abscission. In addition, we have recently proposed a third cellular mechanism where the midbody mislocalization is achieved through cytokinesis acceleration driven by the cancer-promoting phosphatase of regenerating liver (PRL)-3. Here we critically review these findings, and we furthermore present new data indicating that midbodies themselves might act as signal unit for polarization since they can infer apical characteristics to a basal membrane.

The post-abscission midbody is an intracellular signaling organelle that regulates cell proliferation

“…We show that internalization of post-mitotic MBs leads to an increase in proliferation in HeLa as well as MDA-MB-31 cell lines, supportive of the idea that post-abscission MB signaling is not just a Hela cell phenomenon but likely functions in other cell types as well. Consistently, recently published work from Lujan and colleagues demonstrated that post-abscission MBs can also regulate epithelial cell polarity in MDCK cells 41 . Based on all of these findings we propose that internalized MBs are long-lived signaling structures which affect several cellular structures and refer to them as MB-containing endosomes or MBsomes (Fig.…”

Separable mechanisms drive local and global polarity establishment in the C. elegans intestinal epithelium

“…The mechanisms required for early local polarization of lateral puncta are unknown. Unlike in MDCK cysts, midbodies are unlikely to provide a polarizing cue since they are positioned on opposite membranes from lateral puncta (Bai et al, 2020; Li et al, 2014; Lujan et al, 2017). Instead, mitosis from E8 to E16 may promote formation of lateral puncta by trafficking polarity proteins along astral microtubules to their lateral attachment sites or by increasing the concavity of the cell membrane which can promote local accumulation of polarity proteins (Chiou et al, 2017; Feldman and Priess, 2012).…”

Insane in the apical membrane: Trafficking events mediating apicobasal epithelial polarity during tube morphogenesis

“…3). Interestingly, this mechanism of cell-division linked lumenogenesis appears to be conserved in other specialized epithelial cell types, such as hepatocytes 24 and human intestinal cells 25 .…”