Daniel N. Stephen

The paper identifies a rare Nestin-expressing granule cell precursor subpopulation that drives SHH medulloblastoma formation with high tumorigenic efficiency.

This study shows adult Nestin+ cerebellar astroglia have limited regenerative potential compared to neonatal cells, with ATAC-seq revealing developmental gene silencing as a key factor.

This study identifies SP5 and SP8 as transcription factors that drive primary cilia formation through genetic and transcriptomic analyses in mouse embryos.

This study shows that reactive oxygen species (ROS) increase in the neonatal cerebellum after injury, and reducing ROS impairs regenerative processes.

This study shows that PTEN loss accelerates SHH medulloblastoma growth through both cell-autonomous and nonautonomous mechanisms in mouse models.

This study shows that ablating cerebellar output neurons has less impact on behavior than genetic mutations in these neurons, which cause additional deficits in learning and memory.

The paper identifies molecular subdomains in the medial excitatory cerebellar nucleus (eCNm) and shows that En1/2 mutations disrupt their development and survival.

The paper identifies a transitory cell state driven by ASCL1 that enables neural reprogramming in the injured neonatal brain.

The paper describes the development of genetic mouse lines and tools for inducible and reversible intersectional misexpression of genes with high spatiotemporal control.

The paper shows that deleting GLI2 in cerebellar granule cell precursors does not cause severe cerebellar hypoplasia, as NEPs compensate by replenishing GCPs.