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Axon fasciculation defects and retinal dysplasias in mice lacking the immunoglobulin superfamily adhesion molecule BEN/ALCAM/SC1.

The immunoglobulin superfamily adhesion molecule BEN (other names include ALCAM, SC1, DM-GRASP, neurolin, and CD166) has been implicated in the control of numerous developmental and pathological processes, including the guidance of retinal and motor axons to their targets. To test hypotheses about BEN function, we disrupted its gene via homologous recombination and analyzed the resulting mutant mice. Mice lacking BEN are viable and fertile, and display no external morphological defects. Despite grossly normal trajectories, both motor and retinal ganglion cell axons fasciculated poorly and were occasionally misdirected. In addition, BEN mutant retinae exhibited evaginated or invaginated regions with photoreceptor ectopias that resembled the "retinal folds" observed in some human retinopathies. Together, these results demonstrate that BEN promotes fasciculation of multiple axonal populations and uncover an unexpected function for BEN in retinal histogenesis.

Pubmed ID: 15345243

Authors

  • Weiner JA
  • Koo SJ
  • Nicolas S
  • Fraboulet S
  • Pfaff SL
  • Pourquié O
  • Sanes JR

Journal

Molecular and cellular neurosciences

Publication Data

September 3, 2004

Associated Grants

None

Mesh Terms

  • Activated-Leukocyte Cell Adhesion Molecule
  • Animals
  • Cell Adhesion
  • Cell Communication
  • Cell Differentiation
  • Cells, Cultured
  • Choristoma
  • Growth Cones
  • Mice
  • Mice, Knockout
  • Motor Neurons
  • Optic Nerve
  • Retinal Dysplasia
  • Retinal Ganglion Cells