Loss of Dcc in the spinal cord is sufficient to cause a deficit in lateralized motor control and the switch to a hopping gait

Dev Dyn. 2018 Apr;247(4):620-629. doi: 10.1002/dvdy.24549. Epub 2018 Feb 5.


Background: Humans with heterozygous mutations in the axon guidance receptor DCC display congenital mirror movements (MMs), which are involuntary movements of body parts, such as fingers, on one side of the body that mirror voluntary movement of the opposite side. In mice, the homozygous Dcckanga mutant allele causes synchronous MM-like hindlimb movements during locomotion, resulting in hopping. In both human and mice, the neuroanatomical defect responsible for the deficit in lateralized motor control remains to be elucidated.

Results: Using the HoxB8-Cre line to specifically remove Dcc from the spinal cord, we found misrouting of commissural axons during their migration toward the floor plate, resulting in fewer axons crossing the midline. These mice also have a hopping gait, indicating that spinal cord guidance defects alone are sufficient to cause hopping.

Conclusions: Dcc plays a role in the development of local spinal networks to ensure proper lateralization of motor control during locomotion. Local spinal cord defects following loss of Dcc cause a hopping gait in mice and may contribute to MM in humans. Developmental Dynamics 247:620-629, 2018. © 2017 Wiley Periodicals, Inc.

Keywords: DCC; axon guidance; commissural axons; gait; left-right coordination; locomotion; mirror movements; neural circuits; spinal cord.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • DCC Receptor / deficiency
  • DCC Receptor / genetics*
  • Functional Laterality
  • Gait
  • Humans
  • Locomotion
  • Mice
  • Spinal Cord / physiopathology*


  • DCC Receptor
  • Dcc protein, mouse

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