Injury-induced ASCL1 expression orchestrates a transitory cell state required for repair of the neonatal cerebellum.

ABSTRACT: To understand repair processes, it is critical to identify the molecular foundations underlying progenitor diversity and plasticity. Upon injury to the neonatal cerebellum, a normally gliogenic nestin-expressing progenitor (NEP) in the Bergmann glia layer (BgL) undergoes adaptive reprograming to restore granule cell production. However, the cellular states and genes regulating the NEP fate switch are unknown. Using single-cell RNA sequencing and fate mapping, we defined molecular subtypes of NEPs and their lineages under homeostasis and repair. NEPs contain two major subtypes: Hopx⁺ astrogliogenic and Ascl1⁺ neurogenic NEPs that are further subdivided based on their location, lineage, and differentiation status. Upon injury, an Ascl1^+<

SUBMITTER: Bayin NS 

PROVIDER: S-EPMC8654303 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature