Kuebler Chloe A, Paré Adam C
Department of Biological Sciences, University of Arkansas, Fayetteville, AR 72701, USA.
Symmetry (Basel). 2023 Aug;15(8). doi: 10.3390/sym15081490. Epub 2023 Jul 27.
Planar polarity is a commonly observed phenomenon in which proteins display a consistent asymmetry in their subcellular localization or activity across the plane of a tissue. During animal development, planar polarity is a fundamental mechanism for coordinating the behaviors of groups of cells to achieve anisotropic tissue remodeling, growth, and organization. Therefore, a primary focus of developmental biology research has been to understand the molecular mechanisms underlying planar polarity in a variety of systems to identify conserved principles of tissue organization. In the early embryo, the germband neuroectoderm epithelium rapidly doubles in length along the anterior-posterior axis through a process known as convergent extension (CE); it also becomes subdivided into tandem tissue compartments through the formation of compartment boundaries (CBs). Both processes are dependent on the planar polarity of proteins involved in cellular tension and adhesion. The enrichment of actomyosin-based tension and adherens junction-based adhesion at specific cell-cell contacts is required for coordinated cell intercalation, which drives CE, and the creation of highly stable cell-cell contacts at CBs. Recent studies have revealed a system for rapid cellular polarization triggered by the expression of leucine-rich-repeat (LRR) cell-surface proteins in striped patterns. In particular, the non-uniform expression of Toll-2, Toll-6, Toll-8, and Tartan generates local cellular asymmetries that allow cells to distinguish between cell-cell contacts oriented parallel or perpendicular to the anterior-posterior axis. In this review, we discuss (1) the biomechanical underpinnings of CE and CB formation, (2) how the initial symmetry-breaking events of anterior-posterior patterning culminate in planar polarity, and (3) recent advances in understanding the molecular mechanisms downstream of LRR receptors that lead to planar polarized tension and junctional adhesion.
平面极性是一种普遍观察到的现象，即蛋白质在其亚细胞定位或跨组织平面的活性中表现出一致的不对称性。在动物发育过程中，平面极性是协调细胞群行为以实现各向异性组织重塑、生长和组织的基本机制。因此，发育生物学研究的一个主要重点是了解各种系统中平面极性背后的分子机制，以确定组织组织的保守原则。在早期胚胎中，胚带神经外胚层上皮通过一种称为汇聚延伸（CE）的过程沿前后轴迅速延长一倍；它还通过形成隔室边界（CBs）被细分为串联的组织隔室。这两个过程都依赖于参与细胞张力和粘附的蛋白质的平面极性。基于肌动球蛋白的张力和基于粘着连接的粘附在特定细胞间接触处的富集是协调细胞插入所必需的，细胞插入驱动CE，并在CBs处形成高度稳定的细胞间接触。最近的研究揭示了一种由富含亮氨酸重复（LRR）细胞表面蛋白以条纹模式表达触发的快速细胞极化系统。特别是，Toll-2、Toll-6、Toll-8和Tartan的不均匀表达产生局部细胞不对称性，使细胞能够区分平行或垂直于前后轴的细胞间接触。在这篇综述中，我们讨论了（1）CE和CB形成的生物力学基础，（2）前后模式形成的初始对称性破缺事件如何最终导致平面极性，以及（3）在理解LRR受体下游导致平面极化张力和连接粘附的分子机制方面的最新进展。
