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平面细胞极性的调节由斯默夫乌比基因合酶

Masahiro Narimatsu¹, Rohit Bose, Melanie Pye

¹Center for Systems Biology, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, ON, Canada, M5G 1X5.

|April 22, 2009

概括

松鼠,无素连接酶,意外地控制平面细胞极性 (PCP) 和收/延伸 (CE) 运动. 它们针对Prickle1,将非正规的Wnt信号与脊椎动物发育中的PCP和CE联系起来.

科学领域:

发育生物学发展生物学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

平面细胞极性 (PCP) 对动物发育至关重要,指导细胞和组织组织.
在脊椎动物中,PCP通过收和延伸 (CE) 运动调节感官细胞对齐和神经管闭合.
非正规的Wnt信号通路是已知的PCP和CE的调节者,但它们的精确分子基础尚未完全理解.

研究的目的:

为了研究鼠在调节平面细胞极性 (PCP) 和收/延伸 (CE) 运动中所起的作用.
阐明小猩猩影响这些发育过程的分子机制.

主要方法:

使用了在Smurf1和Smurf2基因中发生突变的小鼠模型.
检查了耳立体对齐 (PCP) 和神经管闭合 (CE) 的缺陷.
通过生物化学测试,研究了小猩猩与核心PCP组件的相互作用,特别是Prickle1.

主要成果:

缺少Smurf1和Smurf2的小鼠表现出尾中的显著PCP缺陷和CE缺陷,包括神经管闭合失败.
研究人员发现,松鼠通过ubiquitination将关键的PCP蛋白质Prickle1作为目标,以降解.
这种行动使得蝶处于非正规的Wnt信号通路中,这对于PCP和CE至关重要.

结论:

松鼠泛素酶在控制PCP和CE方面发挥着至关重要的,以前未被认可的作用.
松鼠作为非正规的Wnt信号与PCP和CE的调节之间的机械联系,通过降解Prickle1.
这些发现为脊椎动物的形态发生和细胞极性分子控制提供了新的见解.

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