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Axonal Degeneration Is Regulated by a Transcriptional Program that Coordinates Expression of Pro- and

Maya Maor-Nof1, Erez Romi1, Hadas Sar Shalom1

  • 1Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot 76100, Israel.

Neuron
|November 28, 2016
PubMed

Insights

Dual specificity phosphatase Dusp16 protects sensory neuron axons from degeneration during development. Dusp16 antagonizes p53 and Puma, preserving axonal integrity and skin innervation.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Developmental Biology

Background:

  • Neuronal cell death and axonal elimination are critical developmental processes.
  • The transcriptional programs governing these events and their components are not fully understood.

Purpose of the Study:

  • To identify novel factors involved in developmental axonal elimination.
  • To elucidate the function and mechanism of dual specificity phosphatase Dusp16 in sensory neuron development.

Main Methods:

  • Transcriptome analysis of sensory neurons under trophic deprivation.
  • Gene knockout studies of Dusp16 and Puma in mice.
  • Assessment of axonal degeneration, innervation, and neuronal survival.

Main Results:

  • Dusp16 was identified in the trophic deprivation-induced transcriptome.
  • Dusp16 deficiency exacerbated axonal degeneration and reduced skin innervation.
  • Dusp16 negatively regulates p53 and antagonizes Puma expression.
  • Simultaneous knockout of Puma and Dusp16 rescued axonal degeneration and innervation deficits.

Conclusions:

  • Dusp16 acts as an axonal preserving factor during development.
  • Physiological axonal elimination involves a transcriptional program integrating regressive and progressive elements.
  • Dusp16's mechanism involves the p53-Puma pathway.
Keywords:
Dusp16NGFPumaaxon degenerationaxon pruningcell deathneurotrophinp53

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