The homeodomain factor Gbx1 is required for locomotion and cell specification in the dorsal spinal cord

PeerJ. 2013 Aug 29:1:e142. doi: 10.7717/peerj.142. eCollection 2013.

Abstract

Dorsal horn neurons in the spinal cord integrate and relay sensory information to higher brain centers. These neurons are organized in specific laminae and different transcription factors are involved in their specification. The murine homeodomain Gbx1 protein is expressed in the mantle zone of the spinal cord at E12.5-13.5, correlating with the appearance of a discernable dorsal horn around E14 and eventually defining a narrow layer in the dorsal horn around perinatal stages. At postnatal stages, Gbx1 identifies a specific subpopulation of GABAergic neurons in the dorsal spinal cord. We have generated a loss of function mutation for Gbx1 and analyzed its consequences during spinal cord development. Gbx1 (-/-) mice are viable and can reproduce as homozygous null mutants. However, the adult mutant mice display an altered gait during forward movement that specifically affects the hindlimbs. This abnormal gait was evaluated by a series of behavioral tests, indicating that locomotion is impaired, but not muscle strength or motor coordination. Molecular analysis showed that the development of the dorsal horn is not profoundly affected in Gbx1 (-/-) mutant mice. However, analysis of terminal neuronal differentiation revealed that the proportion of GABAergic inhibitory interneurons in the superficial dorsal horn is diminished. Our study unveiled a role for Gbx1 in specifying a subset of GABAergic neurons in the dorsal horn of the spinal cord involved in the control of posterior limb movement.

Keywords: GABAergic neurons; Gbx genes; Locomotion; Mouse mutant; Spinal cord.

Grants and funding

This work was supported by grants from the Agence Nationale de la Recherche (ANR Neurosciences 2007, ANR Blanc 2011), the Fondation pour la Recherche Médicale (Equipe FRM 2007), the Deutsche Forschungsgemeinschaft (SFB-655 A3-Brand), the Italian Association for Cancer Research (AIRC), and by institutional funding from the Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM), and University of Strasbourg. Behavioral phenotyping was partly subsidized by the EUMODIC European Consortium and the Mouse Clinical Institute (MCI/ICS, Strasbourg). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.