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Chapter 3 - Cell Polarity and Asymmetric Cell Division by the Wnt Morphogen
Book chapter

Chapter 3 - Cell Polarity and Asymmetric Cell Division by the Wnt Morphogen

Austin T Baldwin and Bryan T Phillips
Cell Polarity in Development and Disease, pp.61-102
Elsevier Inc
2018
DOI: 10.1016/B978-0-12-802438-6.00003-6

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Abstract

All multicellular organisms require molecular mechanisms that create cellular diversity during both embryonic development as well as adult tissue homeostasis. One critical and conserved method of achieving this diversity is binary cell fate specification via asymmetric cell division (ACD). Asymmetric division of polarized mother cells results in the unequal inheritance of cell fate determinants that in turn generate two different cell types that can now give rise to developmentally distinct tissues. ACD can also be used to maintain populations of cells in adult tissues, as stem cells can divide asymmetrically to produce a new stem cell daughter as well as a daughter cell that terminally differentiates to maintain tissue integrity. Here, we review different modes of ACD, focusing on a pathway driven by the Wnt morphogen, termed the Wnt/β-catenin asymmetry (WβA) pathway, as a well-understood example of cell polarization by a morphogen gradient. The WβA pathway polarizes many cell divisions through the development nematode Caenorhabditis elegans, resulting in the formation of two daughters with distinct transcriptional profiles due to asymmetric regulation of the β-catenins, SYS-1 and WRM-1, and the T-cell factor transcription factor, POP-1. We discuss the signal transduction adaptations present in WβA as compared to the “canonical” Wnt/β-catenin signaling pathway that has powered WβA specialization for ACD regulation. Since Wnt/β-catenin signaling is implicated in developmental defects and various cancers, we discuss how the lessons learned from WβA can be harnessed to better understand the canonical Wnt/β-catenin pathway.
Asymmetric cell division POP-1/TCFSYS-1 Wnt/beta-catenin WRM-1

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