The postmitotic midbody: Regulating polarity, stemness, and proliferation

Abstract

Abscission, the final stage of cell division, requires well-orchestrated changes in endocytic trafficking, microtubule severing, actin clearance, and the physical sealing of the daughter cell membranes. These processes are highly regulated, and any missteps in localized membrane and cytoskeleton dynamics often lead to a delay or a failure in cell division. The midbody, a microtubule-rich structure that forms during cytokinesis, is a key regulator of abscission and appears to function as a signaling platform coordinating cytoskeleton and endosomal dynamics during the terminal stages of cell division. It was long thought that immediately following abscission and the conclusion of cell division, the midbody is either released or rapidly degraded by one of the daughter cells. Recently, the midbody has gained prominence for exerting postmitotic functions. In this review, we detail the role of the midbody in orchestrating abscission, as well as discuss the relatively new field of postabscission midbody biology, particularly focusing on how it may act to regulate cell polarity and its potential to regulate cell tumorigenicity or stemness.

The ARF GAP ELMOD2 acts with different GTPases to regulate centrosomal microtubule nucleation and cytokinesis

“…The later stages of cytokinesis, including abscission, require the selective recruitment of multiple regulatory proteins to key sites (including centrosomes, cleavage furrows, recycling endosomes, and midbodies) via mechanisms that are often incompletely understood ( Agromayor and Martin-Serrano, 2013 ; Nakayama, 2016 ; Nahse et al. , 2017 ; Peterman and Prekeris, 2019 ). Such proteins may traffic to the mitotic spindle or cleavage furrow during metaphase and anaphase, and later to specific parts of the midbody to facilitate abscission.…”

A Model for Primary Cilium Biogenesis by Polarized Epithelial Cells: Role of the Midbody Remnant and Associated Specialized Membranes

“…Severing of the MB membrane causes the physical separation of the two daughter cells in a process named abscission (Mierzwa and Gerlich, 2014 ). Following abscission, the FB and the remainder of the arms form an MB remnant (MBR) that is either released into the extracellular space, in cases where the MB membrane is cleaved in the two arms, or is inherited by one of the daughter cells, when the cleavage occurs in only one of the arms (Chen et al, 2012 ; Peterman and Prekeris, 2019 ).…”

Exovesicular-Shh confers Imatinib resistance by upregulating Bcl2 expression in chronic myeloid leukemia with variant chromosomes

“…We deliberate that the presence of primary ciliumlike structures could rather represent post-mitotic midbody. Midbodies are retracted in most cells post mitosis via phagocytosis but can be retained in some post-mitotic cells for functions other than cytokinesis 27,28 . Primary cilium is required for Shh signaling but there are also exceptions [29][30][31][32] .…”