Abstract
The formation of the neocortex relies on intracellular and extracellular signaling molecules that are involved in the sequential steps of corticogenesis, ranging from the proliferation and differentiation of neural progenitor cells to the migration and dendrite formation of neocortical neurons. Abnormalities in these steps lead to disruption of the cortical structure and circuit, and underly various neurodevelopmental diseases, including dyslexia and autism spectrum disorder (ASD). In this review, we focus on the axon guidance signaling Slit-Robo, and address the multifaceted roles of Slit-Robo signaling in neocortical development. Recent studies have clarified the roles of Slit-Robo signaling not only in axon guidance but also in progenitor cell proliferation and migration, and the maturation of neocortical neurons. We further discuss the etiology of neurodevelopmental diseases, which are caused by defects in Slit-Robo signaling during neocortical formation.
Highlights
The neocortex is the six-layered outermost structure of the cerebrum, and is considered to be an evolutionarily new region of the brain that appeared soon after the emergence of mammals
We focus on Slit and Robo, which were originally identified as axon guidance molecules, and discuss the novel roles of Slit-Robo signaling in neocortical development
ROBO plays a crucial role in human neocortical development by regulating dendrite formation and neuron positioning, and such abnormalities occurring in language-associated regions can lead to dyslexia
Summary
The neocortex is the six-layered outermost structure of the cerebrum, and is considered to be an evolutionarily new region of the brain that appeared soon after the emergence of mammals. The remaining Ig domains in the hypomorphic Robo1 mutant mice may affect the number of aRGCs. The function of Robo in cortical progenitor cells has been mediated by a crosstalk between Robo signaling and Hes1, which is a transcription factor acting downstream of Notch (Borrell et al, 2012, Figure 1).
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