Karol Cichewicz

This study examines the effects of Chd8 haploinsufficiency on cerebellar development and function in mice, revealing cell-type-specific transcriptomic and physiological changes.

The paper develops murine and zebrafish Wac deletion models to study DeSanto-Shinawi Syndrome, finding craniofacial, behavioral, and neurodevelopmental phenotypes similar to the human condition.

The paper presents a model of dynamic spatial and temporal patterning in the embryonic basal ganglia, showing how progenitor movement and transcriptional changes lead to diverse neuronal subtypes.

The paper identifies how uneven SNP distribution on the X-chromosome of Drosophila affects meiotic crossover sites, reducing mapping resolution for genetic traits.

The paper identifies CHD8 interactions in mouse brain, revealing a role in chromatin-associated RNA processing and highlighting dosage sensitivity in neurodevelopmental disorders.

This study identifies persistent excitatory neuron dysfunction in Chd8 haploinsufficient mice through single nucleus transcriptomics and behavioral analysis.

The paper identifies combinatorial TF-cRE interactions in mouse basal ganglia development, revealing modules that drive GABAergic neurogenesis and suppress other fates.

The paper identifies and validates enhancers active in early postnatal mouse brain using a modified MPRA approach and rAAV delivery.

This study identifies transcriptomic and neuroanatomical changes in mouse embryos exposed to maternal immune activation, revealing altered neurodevelopmental timing and cortical development.

The paper shows nitric oxide acts as a cotransmitter in dopaminergic neurons to modulate memory dynamics in Drosophila.

The paper uses a genetic model to study transcriptome changes in dopamine-depleted mice, finding DA-dependent gene expression in SNc that suggests a protective role for dopamine.