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ASF/SF2调节的CaMKIIdelta替代拼接暂时重新编程心肌中的刺激-收缩合

Xiangdong Xu¹, Dongmei Yang, Jian-Hua Ding

¹Department of Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.

|January 18, 2005

概括

一个涉及拼接因子ASF/SF2的新型拼接程序对于产后心脏重塑至关重要. 这个程序中的缺陷,特别是CaMKIIdelta拼接,会在小鼠中引起严重的心脏收缩缺陷.

科学领域:

分子生物学分子生物学
心血管生物学心血管生物学
发展生物学发展生物学

背景情况:

生物在从青少年到成年生活的过渡期间经历了编程组织重塑,以适应环境需求.
替代拼接是控制基因表达和蛋白质多样性的关键调节机制,在发育过程中.

研究的目的:

确定涉及产后心脏重塑的新型替代拼接程序.
研究拼接因子ASF/SF2在调节这些程序中的作用.
阐明异常拼接在心脏发育中的功能后果.

主要方法:

使用了患有ASF/SF2.2心肌细胞特异性缺陷的小鼠模型.
在发育中的心脏中分析了替代拼接事件.
在心肌细胞中研究了Ca2+/calmodulin依赖激酶IIdelta (CaMKIIdelta) 的定位和功能.

主要成果:

确定了一项监管的替代拼接程序,该程序对于产后心脏重塑至关重要,由ASF/SF2.2调解.
缺少ASF/SF2的心肌细胞由于有缺陷的CaMKIIdelta拼接而表现出过度收缩.
将CaMKIIdelta错误地向了sarcolemmal膜,导致了严重的刺激 - 收缩合缺陷.

结论:

ASF/SF2是心脏重编程通路中的基本拼接调节器.
ASF/SF2调节的CaMKIIdelta替代拼接对于发育中的心脏的功能重塑至关重要.
异常拼接在产后发育期间有助于心脏功能障碍.

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