The Notch signaling pathway controls the size of the ocular lens by directly suppressing p57Kip2 expression
The Notch signaling pathway controls the size of the ocular lens by directly suppressing p57Kip2 expression
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DOI：
10.1128/mcb.00780-07
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发表时间：
2007-10-01
影响因子：
5.3
通讯作者：
Zhang, Pumin
中科院分区：
文献类型：
--
作者：
Jia, Junling;Lin, Min;Zhang, Pumin
器官的大小必须严格控制，以使其适合有机体。哺乳动物晶状体是一种相对简单的器官，由终末分化的无丝分裂晶状体纤维细胞组成，其前表面覆盖有一层未成熟的有丝分裂上皮细胞。晶状体上皮细胞的增殖促进晶状体的生长，从而控制晶状体的大小。我们报告说，Notch 信号通路定义了发育中晶状体增殖和分化之间的界限。 Notch 信号传导的丧失导致上皮细胞无法分化并且晶状体变得更小。我们发现Notch效应器Herp2在晶状体上皮中表达，并直接抑制p57（Kip2）的表达，在晶状体发育过程中提供Notch信号传导和细胞周期控制机制之间的分子联系。
The size of an organ must be tightly controlled so that it fits within an organism. The mammalian lens is a relatively simple organ composed of terminally differentiated, amitotic lens fiber cells capped on the anterior surface by a layer of immature, mitotic epithelial cells. The proliferation of lens epithelial cells fuels the growth of the lens, thus controlling the size of the lens. We report that the Notch signaling pathway defines the boundary between proliferation and differentiation in the developing lens. The loss of Notch signaling results in the loss of epithelial cells to differentiation and a much smaller lens. We found that the Notch effector Herp2 is expressed in lens epithelium and directly suppresses p57(Kip2) expression, providing a molecular link between Notch signaling and the cell cycle control machinery during lens development.