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一种新型平面极性基因胃蛋白酶原样蛋白以转录后方式调节无翅基因的表达。

A novel planar polarity gene pepsinogen-like regulates wingless expression in a posttranscriptional manner.

作者信息

Mouri Kousuke, Nishino Yutaro, Arata Masaki, Shi Dongbo, Horiuchi Shin-Ya, Uemura Tadashi

机构信息

Graduate School of Biostudies, Kyoto University, Kyoto, Japan.

出版信息

Dev Dyn. 2014 Jun;243(6):791-9. doi: 10.1002/dvdy.24112. Epub 2014 Feb 17.

Abstract

BACKGROUND

Planar cell polarity (PCP) originally referred to the coordination of global organ axes and individual cell polarity within the plane of the epithelium. More recently, it has been accepted that pertinent PCP regulators play essential roles not only in epithelial sheets, but also in various rearranging cells.

RESULTS

We identified pepsinogen-like (pcl) as a new planar polarity gene, using Drosophila wing epidermis as a model. Pcl protein is predicted to belong to a family of aspartic proteases. When pcl mutant clones were observed in pupal wings, PCP was disturbed in both mutant and wild-type cells that were juxtaposed to the clone border. We examined levels of known PCP proteins in wing imaginal discs. The amount of the seven-pass transmembrane cadherin Flamingo (Fmi), one of the PCP "core group" members, was significantly decreased in mutant clones, whereas neither the amount of nor the polarized localization of Dachsous (Ds) at cell boundaries was affected. In addition to the PCP phenotype, the pcl mutation caused loss of wing margins. Intriguingly, this was most likely due to a dramatic decrease in the level of Wingless (Wg) protein, but not due to a decrease in the level of wg transcripts.

CONCLUSIONS

Our results raise the possibility that Pcl regulates Wg expression post-transcriptionally, and PCP, by proteolytic cleavages.

摘要

背景

平面细胞极性(PCP)最初指上皮平面内整体器官轴与单个细胞极性的协调。最近,人们认识到相关的PCP调节因子不仅在上皮细胞层中起重要作用,在各种重排细胞中也起重要作用。

结果

我们以果蝇翅表皮为模型,鉴定出类胃蛋白酶原(pcl)作为一个新的平面极性基因。Pcl蛋白预计属于天冬氨酸蛋白酶家族。当在蛹翅中观察到pcl突变克隆时,与克隆边界相邻的突变细胞和野生型细胞中的PCP均受到干扰。我们检测了翅成虫盘已知PCP蛋白的水平。PCP“核心组”成员之一的七次跨膜钙黏蛋白Flamingo(Fmi)的量在突变克隆中显著降低,而细胞边界处的Dachsous(Ds)的量及其极化定位均未受影响。除了PCP表型外,pcl突变导致翅边缘缺失。有趣的是,这很可能是由于无翅(Wg)蛋白水平急剧下降,而不是由于wg转录本水平下降。

结论

我们的结果提出了一种可能性,即Pcl通过蛋白水解切割在转录后调节Wg表达以及PCP。

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