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刺突蛋白介导反馈放大以产生不对称平面细胞极性信号。

Prickle mediates feedback amplification to generate asymmetric planar cell polarity signaling.

作者信息

Tree David R P, Shulman Joshua M, Rousset Raphaël, Scott Matthew P, Gubb David, Axelrod Jeffrey D

机构信息

Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, CA 94305, USA.

出版信息

Cell. 2002 May 3;109(3):371-81. doi: 10.1016/s0092-8674(02)00715-8.

DOI:10.1016/s0092-8674(02)00715-8
PMID:12015986
Abstract

Planar cell polarity signaling in Drosophila requires the receptor Frizzled and the cytoplasmic proteins Dishevelled and Prickle. From initial, symmetric subcellular distributions in pupal wing cells, Frizzled and Dishevelled become highly enriched at the distal portion of the cell cortex. We describe a Prickle-dependent intercellular feedback loop that generates asymmetric Frizzled and Dishevelled localization. In the absence of Prickle, Frizzled and Dishevelled remain symmetrically distributed. Prickle localizes to the proximal side of pupal wing cells and binds the Dishevelled DEP domain, inhibiting Dishevelled membrane localization and antagonizing Frizzled accumulation. This activity is linked to Frizzled activity on the adjacent cell surface. Prickle therefore functions in a feedback loop that amplifies differences between Frizzled levels on adjacent cell surfaces.

摘要

果蝇中的平面细胞极性信号传导需要受体卷曲蛋白(Frizzled)以及细胞质蛋白散乱蛋白(Dishevelled)和刺蛋白(Prickle)。在蛹期翅细胞中,从最初的对称亚细胞分布开始,卷曲蛋白和散乱蛋白在细胞皮质的远端高度富集。我们描述了一个依赖刺蛋白的细胞间反馈回路,该回路产生不对称的卷曲蛋白和散乱蛋白定位。在没有刺蛋白的情况下,卷曲蛋白和散乱蛋白保持对称分布。刺蛋白定位于蛹期翅细胞的近端,并结合散乱蛋白的DEP结构域,抑制散乱蛋白的膜定位并拮抗卷曲蛋白的积累。这种活性与相邻细胞表面的卷曲蛋白活性相关。因此,刺蛋白在一个反馈回路中起作用,该回路放大相邻细胞表面卷曲蛋白水平之间的差异。

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