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Aplip1,JIP1 的同源物,调节肌核定位和肌肉稳定性。

Aplip1, the homolog of JIP1, regulates myonuclear positioning and muscle stability.

机构信息

Department of Biology, Boston College, Chestnut Hill, MA 02467, USA.

Department of Biology, Boston College, Chestnut Hill, MA 02467, USA

出版信息

J Cell Sci. 2018 Mar 16;131(6):jcs205807. doi: 10.1242/jcs.205807.

DOI:10.1242/jcs.205807
PMID:29487176
Abstract

During muscle development, myonuclei undergo a complex set of movements that result in evenly spaced nuclei throughout the muscle cell. In , two separate pools of Kinesin and Dynein work in synchrony to drive this process. However, how these two pools are specified is not known. Here, we investigate the role of Aplip1 (the homolog of JIP1, JIP1 is also known as MAPK8IP1), a known regulator of both Kinesin and Dynein, in myonuclear positioning. Aplip1 localizes to the myotendinous junction and has genetically separable roles in myonuclear positioning and muscle stability. In mutant embryos, there was an increase in the percentage of embryos that had both missing and collapsed muscles. Via a separate mechanism, we demonstrate that Aplip1 regulates both the final position of and the dynamic movements of myonuclei. Aplip1 genetically interacts with both Raps (also known as Pins) and Kinesin to position myonuclei. Furthermore, Dynein and Kinesin localization are disrupted in Aplip1 mutants suggesting that Aplip1-dependent nuclear positioning requires Dynein and Kinesin. Taken together, these data are consistent with Aplip1 having a function in the regulation of Dynein- and Kinesin-mediated pulling of nuclei from the muscle end.This article has an associated First Person interview with the first author of the paper.

摘要

在肌肉发育过程中,肌细胞核经历一系列复杂的运动,导致细胞核在肌肉细胞中均匀分布。在这篇文章中,两个独立的 Kinesin 和 Dynein 池协同工作,推动这个过程。然而,这两个池是如何被指定的还不清楚。在这里,我们研究了 Aplip1(JIP1 的同源物,JIP1 也称为 MAPK8IP1)在肌核定位中的作用,Aplip1 是 Kinesin 和 Dynein 的已知调节剂。Aplip1 定位于肌腱连接处,在肌核定位和肌肉稳定性方面具有遗传上可分离的作用。在 突变体胚胎中,缺失和塌陷肌肉的胚胎比例增加。通过一个单独的机制,我们证明 Aplip1 调节肌核的最终位置和动态运动。Aplip1 与 Raps(也称为 Pins)和 Kinesin 都有遗传相互作用,以定位肌核。此外,在 Aplip1 突变体中,Dynein 和 Kinesin 的定位被破坏,这表明 Aplip1 依赖的核定位需要 Dynein 和 Kinesin。总之,这些数据表明 Aplip1 在调节 Dynein 和 Kinesin 介导的从肌肉末端拉动细胞核的过程中具有功能。这篇文章有一篇与论文第一作者的第一人称访谈。

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J Cell Sci. 2018 Mar 16;131(6):jcs205807. doi: 10.1242/jcs.205807.
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