Alexandra L. Joyner

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

This study shows that NFI proteins regulate radial glial progenitor lifespan and output in a dose-dependent manner, affecting neocortical development and causing malformations in human cerebral organoids and mouse models.

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 investigates how cell division angle affects cerebellar folding by analyzing mouse strains with different folding amounts.

The paper validates the dTAG system for in vivo protein degradation during mammalian development, showing its safety, efficiency, and stage-specific effects on NELFB function.

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

The paper uses scRNA-seq and SCOPE-seq to study adult neurogenesis, identifying NOTUM as a key regulator of V-SVZ NSC differentiation and neurogenesis.

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

This study shows that CSF-1 signaling is essential for cerebellar microglia identity and function, and its disruption causes motor and social behavior defects.

The paper shows cerebellar folding arises from mechanical forces due to uniform cell behavior, not a cellular pre-pattern.

This study shows that YAP, but not TAZ, is required in glial progenitors for cerebellar regeneration after injury in mice.

The paper shows that reduction of cerebellar nuclei neurons leads to proportional scaling down of cerebellar cortex growth due to loss of their presynaptic Purkinje cells.

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

The paper shows that dormant progenitors regenerate Purkinje neurons after injury, but regenerative capacity declines with age.

The paper investigates catch-up growth in fetal mice after inducing cell cycle arrest in chondrocytes, revealing local and systemic compensatory mechanisms that maintain body proportions.