Cytoplasmic dynein and its regulators in neocortical development and disease

Doobin, David J.; Vallee, Richard B.

doi:10.1016/b978-0-12-809470-9.00012-6

Cited by 2 publications

(4 citation statements)

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“…For NDE1 to be a part of this motor complex, it must dimerize with itself or with its paralog NDEL1 (Soares et al, 2012;Bradshaw and Hayashi, 2016). As part of the complex, NDE1 can interact with centromere protein F (CENP-F) at different subcellular localization to control nuclear migration, cell cycle progression, and mitosis (Vergnolle and Taylor, 2007;Bertipaglia et al, 2018;Doobin and Vallee, 2018). A graphical representation of the most prominent NDE1-binding partners and their interacting region in the NDE1 sequence are depicted in Figure 1B.…”

Section: Cellular Functions Of Nde1 and Its Binding Partnersmentioning

confidence: 99%

“…Binding of CenP-F, Nup133, and Nde1 will recruit dynein to form the Nde1/Lis1/dynein motor complex ( Figure 2C'). Specifically, CenP-F acts as an anchor to the nucleus, via its interaction with Nup133, to pull this organelle toward the ventricular surface along the microtubules (Kim et al, 2011;Bertipaglia et al, 2018;Doobin and Vallee, 2018). In turn, these microtubules are anchored at the centrosome, which itself is anchored by the primary cilium (Kim et al, 2011;Spear and Erickson, 2012a,b).…”

Section: Regulation Of Interkinetic Nuclear Migration In Neural Progementioning

confidence: 99%

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

2020

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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.

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