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Abstract：
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 Drosophila 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.
摘要：
平面极性是一种通常观察到的现象，其中蛋白质在其跨组织平面的亚细胞定位或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的基本机制,增长,和组织。因此,发育生物学研究的主要重点是了解各种系统中平面极性的分子机制，以确定组织组织的保守原则。在果蝇早期胚胎中，胚带神经外胚层上皮通过一个称为会聚延伸（CE）的过程，沿着前后轴的长度迅速加倍；它也通过形成隔室边界（CB）而被细分为串联组织隔室。这两个过程都取决于参与细胞张力和粘附的蛋白质的平面极性。在特定的细胞-细胞接触处富集基于肌动球蛋白的张力和基于粘附连接的粘附是协调的细胞嵌入所必需的，驱动CE，并在CB处产生高度稳定的细胞-细胞接触。最近的研究揭示了一种由富含亮氨酸重复序列（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的非均匀表达会产生局部细胞不对称性，从而使细胞能够区分平行或垂直于前后轴的细胞-细胞接触。在这次审查中,我们讨论了(1)CE和CB形成的生物力学基础，（2）前-后图案的初始对称破坏事件如何在平面极性中达到顶峰，和（3）在理解导致平面极化张力和连接粘附的LRR受体下游分子机制方面的最新进展。
