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Cell polarity and extrusion: How to polarize extrusion and extrude misspolarized cells?

Authors :
Staneva R
Levayer R
Source :
Current topics in developmental biology [Curr Top Dev Biol] 2023; Vol. 154, pp. 131-167. Date of Electronic Publication: 2023 Mar 10.
Publication Year :
2023

Abstract

The barrier function of epithelia is one of the cornerstones of the body plan organization of metazoans. It relies on the polarity of epithelial cells which organizes along the apico-basal axis the mechanical properties, signaling as well as transport. This barrier function is however constantly challenged by the fast turnover of epithelia occurring during morphogenesis or adult tissue homeostasis. Yet, the sealing property of the tissue can be maintained thanks to cell extrusion: a series of remodeling steps involving the dying cell and its neighbors leading to seamless cell expulsion. Alternatively, the tissue architecture can also be challenged by local damages or the emergence of mutant cells that may alter its organization. This includes mutants of the polarity complexes which can generate neoplastic overgrowths or be eliminated by cell competition when surrounded by wild type cells. In this review, we will provide an overview of the regulation of cell extrusion in various tissues focusing on the relationship between cell polarity, cell organization and the direction of cell expulsion. We will then describe how local perturbations of polarity can also trigger cell elimination either by apoptosis or by cell exclusion, focusing specifically on how polarity defects can be directly causal to cell elimination. Overall, we propose a general framework connecting the influence of polarity on cell extrusion and its contribution to aberrant cell elimination.<br /> (Copyright © 2023. Published by Elsevier Inc.)

Details

Language :
English
ISSN :
1557-8933
Volume :
154
Database :
MEDLINE
Journal :
Current topics in developmental biology
Publication Type :
Academic Journal
Accession number :
37100516
Full Text :
https://doi.org/10.1016/bs.ctdb.2023.02.010