The p75 neurotrophin receptor prevents the migration of the granule cell precursors away from its mitogenic niche in the external granule layer of the cerebellum, by maintaining a pool of undifferentiated cells capable of responding to mitogenic signals.

Differential expression of 3'UTR isoforms expands regulatory and protein diversity in cerebellar Purkinje and granule cells and during granule cell development.

3D imaging and time-lapse video-microscopy show that the PlexinB2 receptor controls the tempo of granule cell differentiation and sets the pace of their migration in mouse cerebellum.

Nf1 is required during early, but not late, cerebellar development to facilitate neuronal lamination, providing a potential therapeutic prevention strategy for NF1-associated developmental abnormalities.

Human pluripotent stem cell modeling of the ATOH1 lineage identifies a temporal shift in the expression of key transcriptional regulators in the developing human cerebellum, this molecular divergence may drive the protracted development of the human cerebellum compared to rodents.

Mice with Suppressor of Fused mutations have aberrant cerebellar granule cell proliferation accompanied by ectopic expression of an FGF ligand, also expressed in infantile medulloblastoma patients.

Neural progenitors reside in relative low oxygen in the subgranular zone (SGZ), and the higher tissue oxygen levels that these cells must face as they migrate away from the hypoxic areas and differentiate appear to cause oxidative damage and an early phase of cell death.

The first born excitatory cerebellar nuclei neurons influence the survival of their Purkinje cell partners which stimulate the expansion of granule cells and interneurons to produce functional local circuits.

Post-transcriptional control by YTHDC2 is required to turn off the mitotic proliferation program and facilitate proper expression of the meiotic program to allow a clean cell fate transition in the germline stem cell lineage.

Disruption of quality control pathways that function at distinct steps to mitigate errors in translation evoke similar cellular responses and pathologies.