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Plexina4 and cell survival in the developing zebrafish hindbrain.

Zachary W Nurcombe1,2, Carrie Lynn Hehr1, Sarah McFarlane1

  • 1Department Cell Biology and Anatomy, Hotchkiss Brain Institute, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta, Canada.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
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Summary

Plexina4 signaling promotes neuron survival in the developing zebrafish hindbrain. This study investigated Plexina4

Keywords:
CRISPR mutantClusterinapoptosisembryofloor platemotor neuron

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Area of Science:

  • Neuroscience
  • Developmental Biology

Background:

  • Growth factors are crucial for neuronal survival and development.
  • Plexins, Semaphorin receptors, guide axons and blood vessels.
  • The role of developmental signaling molecules in neurogenesis and cell survival is not fully understood.

Purpose of the Study:

  • To investigate the role of Plexina4 in neuronal survival in the developing zebrafish nervous system.
  • To explore the potential involvement of Clusterin as a ligand for Plexina4 in mediating cell survival.

Main Methods:

  • Examined plexina4 expression patterns in embryonic zebrafish hindbrain.
  • Utilized CRISPR technology to create plexina4 mutants and assessed apoptosis levels.
  • Employed morpholino-mediated knockdown to study the effects of Clusterin depletion.
  • Conducted epistasis experiments to determine the relationship between Plexina4 and Clusterin.

Main Results:

  • Plexina4 (plexina4) is widely expressed in the embryonic zebrafish brain, concentrating in the hindbrain.
  • A plexina4 CRISPR mutant exhibited increased apoptosis in the embryonic hindbrain.
  • Clusterin is expressed in the floor plate, near plexina4-expressing cells.
  • Knockdown of Clusterin led to elevated hindbrain apoptosis, exacerbated in plexina4 mutants.

Conclusions:

  • Plexina4 plays a significant role in promoting cell survival within the developing zebrafish hindbrain.
  • The cell-survival promoting function of Plexina4 appears to operate independently of Clusterin.