Topic: neural differentiation

During mammalian neurodevelopment, the establishment of spatial and temporally appropriate gene expression programmes ensures the correct production of distinct neural and glial cell types. This process is partially regulated by the modification of chromatin structure by epigenetic complexes, including the Polycomb group (PcG) family of co-repressors. Genetic screening has identified several PcG mutations that are causally associated with a range of congenital brain disorders, yet the specific regulatory roles of Polycomb complexes during normal neurodevelopment is still unclear. Here, we inve

Schizophrenia (SCZ) is a debilitating psychiatric disorder, affecting approximately 1% of the global population. Estimates of the heritability rate of SCZ range around 80%, suggesting a strong genetic component. Loss-of-function mutations in SETD1A have been linked to both SCZ risk and other neurodevelopmental phenotypes. SETD1A is involved in chromatin remodeling through its function as a H3K4 methyltransferase, but how SETD1A loss-of-function mutations lead to altered brain function remains unclear. In the present study, we aim to gain insight into functional consequences of reduced SETD1A f