Autism- and intellectual disability-associated MYT1L mutation alters human cortical interneuron differentiation, maturation, and physiology
Prakasam and colleagues derived human stem cell models of intellectual and developmental disability (IDD)-associated MYT1L mutation. MYT1L mutation increased progenitor cell-cycle withdrawal, neuronal and synaptic gene expression, morphological complexity, and synapse formation. Later consequences included impaired neuronal maturation, channel gene expression, and function. Genome-wide occupancy and transcriptomic analyses defined MYT1L direct targets that mediate these IDD-associated phenotypes.
Prakasam and colleagues derived human stem cell models of intellectual and developmental disability (IDD)-associated MYT1L mutation. MYT1L mutation increased progenitor cell-cycle withdrawal, neuronal and synaptic gene expression, morphological complexity, and synapse formation. Later consequences included impaired neuronal maturation, channel gene expression, and function. Genome-wide occupancy and transcriptomic analyses defined MYT1L direct targets that mediate these IDD-associated phenotypes.
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