H1 ES cells were obtained from WiCell Research Resources (Wicell, WI); the iPS#1 line was derived from dermal fibroblasts of a Dystrophic epidermolysis bullosa patient carrying homozygous mutations in COL7A1, while the iPS#2 line was derived from dermal fibroblast of a sickle cell anemia patient and genetically corrected by homologous recombination (Sebastiano et al., 2011). This type VII collagen gene is not expressed in neurons, patients with mutations have no brain phenotypes, and our study demonstrates that the mutation of this gene does not affect the molecular and functional properties of Ngn2-mediated iN cells. Both iPS lines were generated by infecting with a floxed polycistronic lentiviral reprogramming vector followed by Cre-mediated loop-out of the reprogramming factors (Sommer et al., 2009). ES and iPS cells were maintained as feeder-free cells in mTeSR™1 medium (Stem Cell Technologies; Xu et al., 2010). Mouse glial cells were cultured from the forebrain of newborn wildtype CD1 mice (Franke et al., 1998). Briefly, newborn mouse forebrain homogenates were digested with papain and EDTA for 30 min, cells were dissociated by harsh trituration to avoid growing of
