Aberrant axonal projections in mice lacking EphA8 (Eek) tyrosine protein kinase receptors

EMBO J. 1997 Jun 2;16(11):3106-14. doi: 10.1093/emboj/16.11.3106.


We have generated mice homozygous for a mutation that disrupts the gene encoding EphA8, a member of the Eph family of tyrosine protein kinase receptors, previously known as Eek. These mice develop to term, are fertile and do not display obvious anatomical or physiological defects. The mouse ephA8/eek gene is expressed primarily in a rostral to caudal gradient in the developing tectum. Axonal tracing experiments have revealed that in these mutant mice, axons from a subpopulation of tectal neurons located in the superficial layers of the superior colliculus do not reach targets located in the contralateral inferior colliculus. Moreover, ephA8/eek null animals display an aberrant ipsilateral axonal tract that projects to the ventral region of the cervical spinal cord. Retrograde labeling revealed that these abnormal projections originate from a small subpopulation of superior colliculus neurons that normally express the ephA8/eek gene. These results suggest that EphA8/Eek receptors play a role in axonal pathfinding during development of the mammalian nervous system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Axons / pathology*
  • Cell Communication
  • Cell Lineage
  • Central Nervous System / embryology*
  • Central Nervous System / pathology
  • Inferior Colliculi / embryology
  • Inferior Colliculi / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Models, Neurological
  • Nerve Tissue Proteins / genetics*
  • Neural Pathways / physiopathology*
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Receptor, EphA8
  • Spinal Cord / embryology
  • Spinal Cord / pathology
  • Superior Colliculi / embryology
  • Superior Colliculi / pathology


  • Nerve Tissue Proteins
  • Receptor Protein-Tyrosine Kinases
  • Receptor, EphA8