Autophagy in Zebrafish Extraocular Muscle Regeneration.

Autophagy in Zebrafish Extraocular Muscle Regeneration.
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DOI:
10.1007/7651_2018_160
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发表时间:
2019
影响因子:
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通讯作者:
A. Saera-Vila;P. Kish;A. Kahana
A. Saera-Vila;P. Kish;A. Kahana
中科院分区:
--
文献类型:
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作者:
A. Saera-Vila;P. Kish;A. Kahana

文献摘要

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斑马鱼眼外肌严重损伤后再生。受损的肌细胞去分化为间充质祖细胞状态,并重新进入细胞周期以增殖、迁移和再分化为功能性肌肉。从充满肌节的多核合胞体肌纤维开始并以增殖的单核成肌细胞结束的去分化过程必须包括细胞的蛋白质机制和细胞器内容物的显著重塑。事实证明,自噬在这个过程的早期起着关键作用,降解肌节以及合胞体多核肌纤维的多余核。由于斑马鱼重编程过程的鲁棒性及其相对同步性,它可以作为研究自噬生物学的有用体内模型。在这一章中,我们描述了手术肌肉损伤模型以及评估和操纵自噬激活的实验方案。
Zebrafish extraocular muscles regenerate after severe injury. Injured myocytes dedifferentiate to a mesenchymal progenitor state and reenter the cell cycle to proliferate, migrate, and redifferentiate into functional muscles. A dedifferentiation process that begins with a multinucleated syncytial myofiber filled with sarcomeres and ends with proliferating mononucleated myoblasts must include significant remodeling of the protein machinery and organelle content of the cell. It turns out that autophagy plays a key role early in this process, to degrade the sarcomeres as well as the excess nuclei of the syncytial multinucleated myofibers. Because of the robustness of the zebrafish reprogramming process, and its relative synchrony, it can serve as a useful in vivo model for studying the biology of autophagy. In this chapter, we describe the surgical muscle injury model as well as the experimental protocols for assessing and manipulating autophagy activation.