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连接蛋白对晶状体发育的独特和冗余贡献。

Unique and redundant connexin contributions to lens development.

作者信息

White Thomas W

机构信息

Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.

出版信息

Science. 2002 Jan 11;295(5553):319-20. doi: 10.1126/science.1067582.

Abstract

Connexin genes encode intercellular channels that help to coordinate development. In mice, the targeted deletion of different connexins produces disparate effects on ocular growth and differentiation in the lens, and the need for multiple channel subunits is poorly understood. Knockout of Cx46 causes a loss of homeostasis and cataracts. Deletion of Cx50 results in reduced ocular growth and cataracts. Targeted replacement of Cx50 with Cx46 by genetic knock-in corrected defects in cellular differentiation and prevented cataracts, but did not restore normal growth. These data show that intrinsic properties of Cx50 were required for cellular growth, whereas nonspecific restoration of communication by Cx46 maintained differentiation.

摘要

连接蛋白基因编码有助于协调发育的细胞间通道。在小鼠中,不同连接蛋白的靶向缺失对晶状体的眼生长和分化产生不同影响,而对多个通道亚基的需求了解甚少。敲除Cx46会导致体内平衡丧失和白内障。敲除Cx50会导致眼生长减缓及白内障。通过基因敲入用Cx46靶向替代Cx50可纠正细胞分化缺陷并预防白内障,但无法恢复正常生长。这些数据表明,Cx50的内在特性是细胞生长所必需的,而Cx46对通讯的非特异性恢复维持了分化。

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