Abstract
Cell polarity refers to the asymmetric distribution of signaling molecules, cellular organelles, and cytoskeleton in a cell. Neural progenitors and neurons are highly polarized cells in which the cell membrane and cytoplasmic components are compartmentalized into distinct functional domains in response to internal and external cues that coordinate polarity and behavior during development and disease. In neural progenitor cells, polarity has a prominent impact on cell shape and coordinate several processes such as adhesion, division, and fate determination. Polarity also accompanies a neuron from the beginning until the end of its life. It is essential for development and later functionality of neuronal circuitries. During development, polarity governs transitions between multipolar and bipolar during migration of postmitotic neurons, and directs the specification and directional growth of axons. Once reaching final positions in cortical layers, neurons form dendrites which become compartmentalized to ensure proper establishment of neuronal connections and signaling. Changes in neuronal polarity induce signaling cascades that regulate cytoskeletal changes, as well as mRNA, protein, and vesicle trafficking, required for synapses to form and function. Hence, defects in establishing and maintaining cell polarity are associated with several neural disorders such as microcephaly, lissencephaly, schizophrenia, autism, and epilepsy. In this review we summarize the role of polarity genes in cortical development and emphasize the relationship between polarity dysfunctions and cortical malformations.
Highlights
Polarity describes structural, biochemical, or functional asymmetry in cells
Adhesion proteins sit at the center of apical junctional complexes (AJCs)
These structures serve as molecular platforms that assemble polarity protein complexes during cell division and orient the mitotic spindle, thereby affecting fate determination of neural progenitors and differentiation of neural cells
Summary
Université catholique de Louvain, Institute of Neuroscience, Developmental Neurobiology, Brussels, Belgium. Reviewed by: Alfonso Represa, INSERM U901 Institut de Neurobiologie de la Méditerranée, France Fiona Francis, INSERM U839 Institut du Fer à Moulin, France. Specialty section: This article was submitted to Cellular Neuropathology, a section of the journal
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