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An expanded cortex is a hallmark of human neurodevelopment and endows increased cognitive capabilities. Recent work has shown that the cell cycle-related gene  NDE1  is essential for proper cortical development. Patients who have mutations in  NDE1  exhibit congenital microcephaly as a primary phenotype. At the cellular level,  NDE1  is essential for interkinetic nuclear migration and mitosis of radial glial cells, which translates to an indispensable role in neurodevelopment. The nuclear migration function of  NDE1  is well conserved across Opisthokonta. In mammals, multiple isoforms containing alternate terminal exons, which influence the functionality of  NDE1 , have been reported. It has been noted that the pattern of terminal exon usage mirrors patterns of cortical complexity in mammals. To provide context to these findings, here, we provide a comprehensive review of the literature regarding  NDE1 , its molecular biology and physiological relevance at the cellular and organismal levels. In particular, we outline the potential roles of  NDE1  in progenitor cell behavior and explore the spectrum of  NDE1  pathogenic variants. Moreover, we assessed the evolutionary conservation of  NDE1  and interrogated whether the usage of alternative terminal exons is characteristic of species with gyrencephalic cortices. We found that gyrencephalic species are more likely to express transcripts that use the human-associated terminal exon, whereas lissencephalic species tend to express transcripts that use the mouse-associated terminal exon. Among gyrencephalic species, the human-associated terminal exon was preferentially expressed by those with a high order of gyrification. These findings underscore phylogenetic relationships between the preferential usage of  NDE1  terminal exon and high-order gyrification, which provide insight into cortical evolution underlying high-order brain functions.

Role of NDE1 in the Development and Evolution of the Gyrified Cortex