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The actin polymerization factor Diaphanous and the actin severing protein Flightless I collaborate to regulate sarcomere size
Developmental Biology ( IF 2.7 ) Pub Date : 2020-09-25 , DOI: 10.1016/j.ydbio.2020.09.014
Su Deng 1 , Ruth L Silimon 2 , Mridula Balakrishnan 2 , Ingo Bothe 1 , Devin Juros 1 , David B Soffar 1 , Mary K Baylies 3
Affiliation  

The sarcomere is the basic contractile unit of muscle, composed of repeated sets of actin thin filaments and myosin thick filaments. During muscle development, sarcomeres grow in size to accommodate the growth and function of muscle fibers. Failure in regulating sarcomere size results in muscle dysfunction; yet, it is unclear how the size and uniformity of sarcomeres are controlled. Here we show that the formin Diaphanous is critical for the growth and maintenance of sarcomere size: Dia sets sarcomere length and width through regulation of the number and length of the actin thin filaments in the Drosophila flight muscle. To regulate thin filament length and sarcomere size, Dia interacts with the Gelsolin superfamily member Flightless I (FliI). We suggest that these actin regulators, by controlling actin dynamics and turnover, generate uniformly sized sarcomeres tuned for the muscle contractions required for flight.



中文翻译:

肌动蛋白聚合因子 Diaphanous 和肌动蛋白切断蛋白 Flightless I 合作调节肌节大小

肌节是肌肉的基本收缩单位,由重复的肌动蛋白细丝和肌球蛋白粗丝组成。在肌肉发育过程中,肌节的大小会增长以适应肌肉纤维的生长和功能。无法调节肌节大小会导致肌肉功能障碍;然而,目前尚不清楚如何控制肌节的大小和均匀度。在这里,我们表明,formin Diaphanous 对肌节大小的生长和维持至关重要:Dia 通过调节果蝇中肌动蛋白细丝的数量和长度来设置肌节的长度和宽度飞行肌肉。为了调节细丝长度和肌节大小,Dia 与凝溶胶蛋白超家族成员 Flightless I (FliI) 相互作用。我们建议这些肌动蛋白调节剂通过控制肌动蛋白动力学和周转,产生大小均匀的肌节,以适应飞行所需的肌肉收缩。

更新日期:2020-10-02
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