PUBLICATION

Scratch2 Prevents Cell Cycle Re-Entry by Repressing miR-25 in Postmitotic Primary Neurons

Authors
Rodríguez-Aznar, E., Barrallo-Gimeno, A., and Nieto, M.A.
ID
ZDB-PUB-130408-9
Date
2013
Source
The Journal of neuroscience : the official journal of the Society for Neuroscience   33(12): 5095-5105 (Journal)
Registered Authors
Barrallo Gimeno, Alejandro, Nieto, Angela, Rodríguez-Aznar, Eva
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/physiology
  • Cell Survival/physiology
  • Cyclin-Dependent Kinase Inhibitor p57/genetics
  • Cyclin-Dependent Kinase Inhibitor p57/metabolism
  • Gene Expression Regulation, Developmental/physiology
  • Gene Knockdown Techniques
  • Green Fluorescent Proteins/genetics
  • Homeostasis/physiology
  • Luminescent Proteins/genetics
  • MicroRNAs/genetics
  • MicroRNAs/physiology*
  • Mitosis/physiology*
  • Neurogenesis/physiology
  • Neurons/cytology
  • Neurons/physiology*
  • Spinal Cord/cytology
  • Spinal Cord/embryology
  • Spinal Cord/physiology
  • Transcription Factors/genetics*
  • Transcription Factors/metabolism*
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism*
PubMed
23516276 Full text @ J. Neurosci.
Abstract

During the development of the nervous system the regulation of cell cycle, differentiation, and survival is tightly interlinked. Newly generated neurons must keep cell cycle components under strict control, as cell cycle re-entry leads to neuronal degeneration and death. However, despite their relevance, the mechanisms controlling this process remain largely unexplored. Here we show that Scratch2 is involved in the control of the cell cycle in neurons in the developing spinal cord of the zebrafish embryo. scratch2 knockdown induces postmitotic neurons to re-enter mitosis. Scratch2 prevents cell cycle re-entry by maintaining high levels of the cycle inhibitor p57 through the downregulation of miR-25. Thus, Scratch2 appears to safeguard the homeostasis of postmitotic primary neurons by preventing cell cycle re-entry.

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