Journal Article

DZNE-2022-01198

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png A Nuclear Belt Fastens on Neural Cell Fate

Mestres, I. ; Houtman, J.DZNE* ; Calegari, F. ; Toda, T. (Last author)DZNE*

2022
MDPI Basel

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Please use a persistent id in citations: doi:10.3390/cells11111761

Abstract: Successful embryonic and adult neurogenesis require proliferating neural stem and progenitor cells that are intrinsically and extrinsically guided into a neuronal fate. In turn, migration of new-born neurons underlies the complex cytoarchitecture of the brain. Proliferation and migration are therefore essential for brain development, homeostasis and function in adulthood. Among several tightly regulated processes involved in brain formation and function, recent evidence points to the nuclear envelope (NE) and NE-associated components as critical new contributors. Classically, the NE was thought to merely represent a barrier mediating selective exchange between the cytoplasm and nucleoplasm. However, research over the past two decades has highlighted more sophisticated and diverse roles for NE components in progenitor fate choice and migration of their progeny by tuning gene expression via interactions with chromatin, transcription factors and epigenetic factors. Defects in NE components lead to neurodevelopmental impairments, whereas age-related changes in NE components are proposed to influence neurodegenerative diseases. Thus, understanding the roles of NE components in brain development, maintenance and aging is likely to reveal new pathophysiological mechanisms for intervention. Here, we review recent findings for the previously underrepresented contribution of the NE in neuronal commitment and migration, and envision future avenues for investigation. View Full-Text

Keyword(s): Cell Differentiation: physiology (MeSH) ; Cell Nucleus (MeSH) ; Neurogenesis: genetics (MeSH) ; Neurons: metabolism (MeSH) ; Nuclear Envelope: metabolism (MeSH)

Note: (CC BY)

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Contributing Institute(s):

1. Nuclear architecture in neural plasticity and aging (AG Toda)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2022

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