Benedikt Berninger

The paper shows that brain injury reactivates a developmental program in astrocytes to generate transient LGE-class interneurons that integrate into neural circuits.

This study shows that astrocytes can be converted into functional neurons in the mouse visual cortex, which can integrate into cortical circuits and respond to visual stimuli.

This study shows that a modified Ascl1 variant, Ascl1SA6, can reprogram glial cells into interneurons that resemble canonical cortical interneurons when combined with Dlx2, improving their laminar positioning.

This study develops an in vitro model of brain injury that recapitulates key features of injury and regeneration, enabling the study of glia-to-neuron reprogramming and stem cell dynamics.

This study reprograms early cortical astroglia into neurons with parvalbumin-positive interneuron features using a modified Ascl1 protein.

The paper shows that reactivation of inactive X-chromosome alleles in female neural cells during differentiation enhances resilience to X-linked neurodevelopmental disorders.

This study shows that Ascl1 induces low-efficiency neuronal reprogramming of proliferative glia in vivo, unlike its efficient in vitro conversion.

This study identifies Yap1 as a regulator of adult neural stem cell activation, showing that its gain-of-function mutant promotes cell cycle entry and aberrant differentiation while wild-type Yap1 does not.

This study identifies transcriptional and chromatin changes during astrocyte maturation in vivo and in culture, showing that extrinsic signals regulate intrinsic transcription factors to drive maturation.

The paper shows neurons and astrocytes in specific brain regions share transcriptional and epigenetic signatures, which are maintained even after reprogramming.

This study shows that forced Neurog2 expression in adult SEZ progenitors reprograms them to generate glutamatergic neurons, but not their postmitotic progeny.