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Non-transport functions of motor proteins in corticogenesis

Aug 2026 · Frontiers in Cell and Developmental Biology · Vol 14 · 0 citations · 244 references
Medicine

TL;DR

The molecular mechanisms that enable dyneins, kinesins, and myosins to function as regulators of cortical development are reviewed and the causal relationship between disruptions to the non-transport functions of motor proteins and cortical developmental disorders is focused on.

Abstract

Cerebral cortex development is a tightly coordinated sequence of interconnected processes: proliferation of neural progenitors, neuronal migration, neurite differentiation, axonal pathfinding, and synaptogenesis. Traditionally, motor proteins–dyneins, kinesins, and myosins–have been viewed as molecules mediating intracellular transport along the cytoskeleton. Nevertheless, data accumulated over the past decade provide compelling evidence for a fundamentally different, non-transport role of these proteins in nervous system development. This review systematizes current understanding of the non-transport functions of motor proteins at key stages of corticogenesis. We review the molecular mechanisms that enable dyneins, kinesins, and myosins to function as regulators of cortical development. We focus specifically on the causal relationship between disruptions to the non-transport functions of motor proteins and cortical developmental disorders, including microcephaly, lissencephaly, and agenesis of the corpus callosum.

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