PUBLICATION

Autophagy in Zebrafish Extraocular Muscle Regeneration

Authors
Saera-Vila, A., Kish, P.E., Kahana, A.
ID
ZDB-PUB-180530-8
Date
2018
Source
Methods in molecular biology (Clifton, N.J.) : (Chapter)
Registered Authors
Kahana, Alon, Kish, Phillip
Keywords
Autolysosome, Autophagy, Cell reprogramming, Dedifferentiation, EOM, Electron microscopy, Extraocular muscle, MMT, Muscle-to-mesenchymal transition, Myectomy, Regeneration, Stem cell, Zebrafish
MeSH Terms
  • Animals
  • Autophagy*
  • Cell Cycle
  • Cell Dedifferentiation
  • Cell Proliferation
  • Cellular Reprogramming
  • Immunohistochemistry
  • Microscopy, Electron, Transmission
  • Models, Biological
  • Oculomotor Muscles/injuries*
  • Oculomotor Muscles/metabolism
  • Oculomotor Muscles/physiology*
  • Regeneration*
  • Zebrafish
PubMed
29797006 Full text @ Meth. Mol. Biol.
Abstract
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.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping