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

• Main Authors: Pablo Lujan, Teresa Rubio, Giulia Varsano, Maja Köhn
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2017-07-01
• Series: Communicative & Integrative Biology
• Subjects: cancer; cell polarity; cytokinesis; epithelia; midbody; PRL-3; PTP4A3
• Online Access: http://dx.doi.org/10.1080/19420889.2017.1338990

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.