Topic: ARID1B

In the first study, we showed that early chronic fluoxetine treatment restore autism-like behavioral abnormalities via excitatory synapse-related transcriptomic reprogramming in ASD-model mouse. We characterized that deletion of ARID1B caused ASD-like behavioral deficits through persistently decreased density of excitatory synapses starting juvenile stage. Pharmacological correction using early chronic fluoxetine treatment targeting first three weeks after birth successfully carried out long-lasing rescue effects on synaptic deficits and behavioral abnormalities. The other study, however, clai

The precise generation of diverse neuronal cell types is crucial for normal brain function. Genetic mutations leading to impaired neuronal development have long been linked to neurodevelopmental disorders. Cerebral organoids can be used to investigate neurodevelopmental disorders in a human context but are limited by variability and low throughput. We have developed the CRISPR-human organoids-scRNA-seq (CHOOSE) system that utilizes verified pairs of gRNAs, inducible CRISPR/Cas9-based genetic disruption, and single-cell transcriptomics for pooled loss-of-function screening in mosaic organoids.