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Profilin1 is required for glial cell adhesion and radial migration of cerebellar granule neurons.


ABSTRACT: Cerebellar granule neurons (CGNs) exploit Bergmann glia (BG) fibres for radial migration, and cell-cell contacts have a pivotal role in this process. Nevertheless, little is known about the mechanisms that control CGN-BG interaction. Here we demonstrate that the actin-binding protein profilin1 is essential for CGN-glial cell adhesion and radial migration. Profilin1 ablation from mouse brains leads to a cerebellar hypoplasia, aberrant organization of cerebellar cortex layers and ectopic CGNs. Conversely, neuronal progenitor proliferation, tangential migration of neurons and BG morphology appear to be independent of profilin1. Our mouse data and the mapping of developmental neuropathies to the chromosomal region of PFN1 suggest a similar function for profilin1 in humans.

SUBMITTER: Kullmann JA 

PROVIDER: S-EPMC3246249 | biostudies-literature | 2011 Dec

REPOSITORIES: biostudies-literature

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Profilin1 is required for glial cell adhesion and radial migration of cerebellar granule neurons.

Kullmann Jan A JA   Neumeyer Alexander A   Gurniak Christine B CB   Friauf Eckhard E   Witke Walter W   Rust Marco B MB  

EMBO reports 20111223 1


Cerebellar granule neurons (CGNs) exploit Bergmann glia (BG) fibres for radial migration, and cell-cell contacts have a pivotal role in this process. Nevertheless, little is known about the mechanisms that control CGN-BG interaction. Here we demonstrate that the actin-binding protein profilin1 is essential for CGN-glial cell adhesion and radial migration. Profilin1 ablation from mouse brains leads to a cerebellar hypoplasia, aberrant organization of cerebellar cortex layers and ectopic CGNs. Con  ...[more]

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