The AMCB group of Neural Differentiation (NEDI) is interested (1) in understanding the cellular and molecular mechanisms that regulate neuronal differentiation and migration during embryonic development; (2) in the involvement of spinal interneurons in the reactive process that follows spinal cord injury in the adult; and (3) in the contribution of spinal interneurons to the initiation and progression of a devastating neurodegenerative pathology, Amyotrophic Lateral Sclerosis.

  1. We initially characterized the roles of a family of homeodomain transcription factors, called Onecut, in the first steps of neuronal development in the embryonic spinal cord. We showed that the Onecut factors are present in most of the spinal populations during development, and that they regulate the production, the diversification, the maintenance, and the migration of some of these cells. Furthermore, we identified factors downstream of the Onecut proteins that are involved in these processes. Finally, we generated animal models to investigate the functions of these factors or to permanently label specific spinal populations. We currently pursue our investigations of the molecular and cellular mechanisms that control these early steps of spinal development
  2. After a lesion of the adult spinal cord, the neural tissue reorganizes to restrain the impact of the injury and to partly restore the altered neural circuits. The participation of numerous neuronal populations in this process, including spinal interneurons, remains unclear. Furthermore, experimental evidence suggest that new neural cells are generated after a spinal cord lesion. Using tools developed to study the development of spinal populations, we address the participation of spinal interneurons to the reactive post-injury process in the adult spinal cord and the possible contribution of new interneurons generated following the lesion.
  3. Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by the death of upper and of lower motor neurons. However, animal models and in vitro or cell transplant studies demonstrated that non-cell autonomous mechanisms involving astrocytes, oligodendrocytes and interneurons contribute or could even be causative of the disease. Yet, the contribution of spinal interneurons to the pathology remains unsolved. We hypothesize that spinal interneurons are either causal agents or modulators of alterations leading to ALS. To address this question, we use different genetic mouse models for assessing the contribution of specific interneuron populations to the induction or the progression of the ALS pathology.

Additional information on the NEDI website