addition, the cells behaved similarly to ESC-derived motor neurons in disease conditions. When cultured with glia carrying the G93A mutation in the Superoxide dismutase (Sod1) gene, a mutation found in familial forms of amyotrophic lateral sclerosis (ALS), the survival of iMN cells decreased. Vice versa, iMN cells derived from Sod1G93A MEFs also showed reduced survival when cultured with wild-type glia. These first translational studies suggest that iMN cells can be used as a tool to understand the pathophysiology of ALS. As a first step in this direction, Son et al. also infected human ESC-derived fibroblast-like cells with the 7 transcription factors in combination with Neurod1. This approach yielded neuronal cells that could fire action potentials and expressed Hb9 and vesicular ChAT. More work is needed to investigate whether iMN cells can be generated from primary human fibroblasts.
