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Planar Asymmetries in the C. elegans Embryo Emerge by Differential Retention of aPARs at Cell-Cell Contacts

机译:秀丽隐杆线虫胚胎的平面不对称通过aPARs在细胞间接触的差异保留而出现。

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摘要

Formation of the anteroposterior and dorsoventral body axis in Caenorhabditis elegans depends on cortical flows and advection of polarity determinants. The role of this patterning mechanism in tissue polarization after formation of cell-cell contacts is not fully understood. Here, we demonstrate that planar asymmetries are established during left-right symmetry breaking: Centripetal cortical flows asymmetrically and differentially advect anterior polarity determinants (aPARs) from contacts to the medial cortex, resulting in their unmixing from apical myosin. Contact localization and advection of PAR-6 requires balanced CDC-42 activation, while asymmetric retention and advection of PAR-3 can occur independently of PAR-6. Concurrent asymmetric retention of PAR-3, E-cadherin/HMR-1 and opposing retention of antagonistic CDC-42 and Wnt pathway components leads to planar asymmetries. The most obvious mark of planar asymmetry, retention of PAR-3 at a single cell-cell contact, is required for proper cytokinetic cell intercalation. Hence, our data uncover how planar polarity is established in a system without the canonical planar cell polarity pathway through planar asymmetric retention of aPARs.
机译:秀丽隐杆线虫的前后体轴的形成取决于皮质流动和极性决定因素的平流。这种构图机制在形成细胞-细胞接触后在组织极化中的作用尚不完全清楚。在这里,我们证明了在左右对称破坏期间建立了平面不对称:向心皮层流不对称且差异地从接触点向内侧皮层平移前极性决定簇(aPAR),从而导致它们从心尖肌球蛋白解开。 PAR-6的接触定位和对流需要平衡的CDC-42激活,而PAR-3的不对称保留和对流可以独立于PAR-6发生。 PAR-3,E-cadherin / HMR-1的同时不对称保留和拮抗性CDC-42和Wnt途径组分的相反保留导致平面不对称。平面不对称性最明显的标志,即PAR-3在单细胞接触中的保留,是适当的细胞动力学细胞嵌入所必需的。因此,我们的数据揭示了如何在没有通过aPAR平面非对称保留的规范平面细胞极性途径的系统中建立平面极性。

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