mitotic spindle deviations, in the mutant cells compared to controls. Such phenotypes were not detected in ASPM mutant mice, which display only mild microcephaly, suggesting that ASPM mechanisms of action may be in part species-specific, underscoring the importance of studying human health in human cells. Moreover, this impairment was not due to the hypothesized defect in proliferation but was more likely the result of perturbed cellular patterning, which could be corrected by applying WNT inhibitor; hence, these models can truly generate novel unexpected mechanistic insights. Finally, Vanderhaegen reported that PSC-derived cortical cells can be transplanted in neonatal mice, where human neurons develop normally but mature at a considerably slower pace than their mouse counterparts (over 9 months instead of 4 weeks), reminiscent of the neoteny that characterizes neuronal maturation in human cortex.
