Loss of SM-B myosin affects muscle shortening velocity and maximal force development
Loss of SM-B myosin affects muscle shortening velocity and maximal force development
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DOI：
10.1038/ncb1101-1025
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发表时间：
2001-11-01
影响因子：
21.3
通讯作者：
Periasamy, M
中科院分区：
文献类型：
--
作者：
Babu, GJ;Loukianov, E;Periasamy, M
我们使用外显子特异性基因靶向策略来产生仅在SM-B肌球蛋白同种型中缺陷的小鼠模型。在这里，我们表明，在平滑肌肌球蛋白的重链基因中的外显子-5B（特定于SM-B）的缺失导致SM-B肌球蛋白的完全丧失和切换剪接的SM-A亚型，而不影响SM 1和SM 2肌球蛋白含量。SM-B肌球蛋白的丢失不影响存活或引起任何明显的平滑肌病理学。生理分析表明，SM-B肌球蛋白的缺乏导致平滑肌组织中最大力产生和缩短速度的显著降低。这是第一个在体内研究，以证明SM-B肌球蛋白亚型的功能作用。我们的结论是额外的7个残基插入SM-B肌球蛋白的表面环1是一个关键的决定因素的横桥循环和缩短的速度。
We used an exon-specific gene-targeting strategy to generate a mouse model deficient only in the SM-B myosin isoform. Here we show that deletion of exon-5B (specific for SM-B) in the gene for the heavy chain of smooth muscle myosin results in a complete loss of SM-B myosin and switching of splicing to the SM-A isoform, without affecting SM1 and SM2 myosin content. Loss of SM-B myosin does not affect survival or cause any overt smooth muscle pathology. Physiological analysis reveals that absence of SM-B myosin results in a significant decrease in maximal force generation and velocity of shortening in smooth muscle tissues. This is the first in vivo study to demonstrate a functional role for the SM-B myosin isoform. We conclude that the extra seven-residue insert in the surface loop 1 of SM-B myosin is a critical determinant of crossbridge cycling and velocity of shortening.