Abstract
Cell polarity is essential for many functions of cells and tissues including the initial establishment and subsequent maintenance of epithelial tissues, asymmetric cell division, and morphogenetic movements. Cell polarity along the apical-basal axis is controlled by three protein complexes that interact with and co-regulate each other: The Par-, Crumbs-, and Scrib-complexes. The localization and activity of the components of these complexes is predominantly controlled by protein-protein interactions and protein phosphorylation status. Increasing evidence accumulates that, besides the regulation at the protein level, the precise expression control of polarity determinants contributes substantially to cell polarity regulation. Here we review how gene expression regulation influences processes that depend on the induction, maintenance, or abolishment of cell polarity with a special focus on epithelial to mesenchymal transition and asymmetric stem cell division. We conclude that gene expression control is an important and often neglected mechanism in the control of cell polarity.
Highlights
Scrib complexes co-localize neuroblasts, and phosphorylation of Dlg1 interacts with the scaffold protein Stardust (Sdt)/PALS1 via its intracellular domain, by aPKC disrupts Dlg1 autoinhibition, which allows it to interact with the spindle which in turn binds to PATJ and Lin-7
The basally formed cell, called ganglion mother cell (GMC), inherits basally localized differentiation factors and divides to produce neurons. Another important player in asymmetric cell division is the adaptor protein Inscuteable (Insc), which is required for apical localization of the Par complex and orients the spindle apparatus by interaction with the microtubule binding protein Mushroom body defective (Mud) and the adaptor protein Partner of Inscuteable (Pins) [26]
Through our literature review we further conclude that transcriptional regulation is decisive for many processes where cell polarity needs to be established, maintained, or abolished
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Epithelial polarity is controlled by three protein complexes that interact and crossThe table lists genes encoding cell polarity their in human,Partitioning. Scrib complexes co-localize neuroblasts, and phosphorylation of Dlg interacts with the scaffold protein Stardust (Sdt)/PALS1 via its intracellular domain, by aPKC disrupts Dlg autoinhibition, which allows it to interact with the spindle which in turn binds to PATJ and Lin-7. The basally formed cell, called ganglion mother cell (GMC), inherits basally localized differentiation factors and divides to produce neurons Another important player in asymmetric cell division is the adaptor protein Inscuteable (Insc), which is required for apical localization of the Par complex and orients the spindle apparatus by interaction with the microtubule binding protein Mushroom body defective (Mud) and the adaptor protein Partner of Inscuteable (Pins) [26]. Besides regulation of apical-basal polarity, aPKC is part of several additional signaling pathways and Scrib is an important regulator of planar cell polarity [37,38]
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