Formation of polarized contractile interfaces by self-organized Toll-8/Cirl GPCR asymmetry.
Formation of polarized contractile interfaces by self-organized Toll-8/Cirl GPCR asymmetry.
复制标题
DOI：
10.1016/j.devcel.2021.03.030
复制
发表时间：
2021-06-07
影响因子：
11.8
通讯作者：
Lecuit T
中科院分区：
文献类型：
--
作者：
Lavalou J;Mao Q;Harmansa S;Kerridge S;Lellouch AC;Philippe JM;Audebert S;Camoin L;Lecuit T
具有不同遗传特性的细胞之间的界面引发信号来组织驱动组织形态发生的局部细胞行为。果蝇胚胎轴的延伸需要肌球蛋白-II的平面极化富集动力定向细胞嵌入。肌球蛋白-II水平定量控制GPCR信号，而肌球蛋白-II极性需要几个Toll受体的模式化表达。Toll受体如何抑制肌球蛋白-II以及这如何涉及GPCR仍然未知。在这里，我们报告说，一个单一的Toll受体，Toll-8的差异表达，极化肌球蛋白-II通过结合到粘附GPCR Cirl/latrophilin。Cirl的不对称表达足以富集肌球蛋白-II，并且Cirl定位在Toll-8表达边界处是不对称的。动态探索的过程中，我们发现，Toll-8和Cirl表现出相互依赖的平面极性响应Toll-8表达相邻细胞之间的定量差异。总的来说，我们提出，细胞表面蛋白质复合物Toll-8/Cirl自组织产生局部非对称界面必不可少的平面极化的收缩性。单个Toll受体的不对称表达导致Myo-II极化。粘附GPCR Cirl结合Toll-8介导Toll-8诱导的Myo-II极化Toll-8边界产生Cirl界面不对称性，其可以抑制Myo-II Toll-8水平的差异导致相互依赖的Toll-8和Cirl平面极性Lavalou，Mao等人。报道Toll-8通过与GPCR Cirl/latrophilin的物理相互作用控制果蝇胚胎和翅盘中的肌球蛋白-II平面极性。他们表明Toll-8表达边界产生Cirl界面不对称性，并提出这是导致肌球蛋白-II极化的潜在信号。
Interfaces between cells with distinct genetic identities elicit signals to organize local cell behaviors driving tissue morphogenesis. The Drosophila embryonic axis extension requires planar polarized enrichment of myosin-II powering oriented cell intercalations. Myosin-II levels are quantitatively controlled by GPCR signaling, whereas myosin-II polarity requires patterned expression of several Toll receptors. How Toll receptors polarize myosin-II and how this involves GPCRs remain unknown. Here, we report that differential expression of a single Toll receptor, Toll-8, polarizes myosin-II through binding to the adhesion GPCR Cirl/latrophilin. Asymmetric expression of Cirl is sufficient to enrich myosin-II, and Cirl localization is asymmetric at Toll-8 expression boundaries. Exploring the process dynamically, we reveal that Toll-8 and Cirl exhibit mutually dependent planar polarity in response to quantitative differences in Toll-8 expression between neighboring cells. Collectively, we propose that the cell surface protein complex Toll-8/Cirl self-organizes to generate local asymmetric interfaces essential for planar polarization of contractility. Asymmetric expression of a single Toll receptor leads to Myo-II polarization The adhesion GPCR Cirl binds to Toll-8 mediating Toll-8-induced Myo-II polarization Toll-8 boundaries generate a Cirl interfacial asymmetry that can polarize Myo-II Differences in Toll-8 levels lead to interdependent Toll-8 and Cirl planar polarity Lavalou, Mao et al. report that Toll-8 controls myosin-II planar polarity in Drosophila embryos and wing discs via a physical interaction with the GPCR Cirl/latrophilin. They show that Toll-8 expression boundaries generate a Cirl interfacial asymmetry and propose that it is a potential signal leading to myosin-II polarization.
登录
查看更多内容
影响因子：
4.6
作者：
Anthoney, Niki;Foldi, Istvan;Hidalgo, Alicia
通讯作者：
Hidalgo, Alicia
影响因子：
11.8
作者：
Hashimoto, Hidehiko;Munro, Edwin
通讯作者：
Munro, Edwin
影响因子：
64.5
作者：
del Toro, Daniel;Carrasquero-Ordaz, Maria A.;Seiradake, Elena
通讯作者：
Seiradake, Elena
影响因子：
11.8
作者：
Alpar L;Bergantiños C;Johnston LA
通讯作者：
Johnston LA
影响因子：
56.9
作者：
Bosveld, Floris;Bonnet, Isabelle;Bellaiche, Yohanns
通讯作者：
Bellaiche, Yohanns