Developmental disruption to the cortical transcriptome and synaptosome in a model of SETD1A loss-of-function.

ABSTRACT: Large-scale genomic studies of schizophrenia implicate genes involved in the epigenetic regulation of transcription by histone methylation and genes encoding components of the synapse. However, the interactions between these pathways in conferring risk to psychiatric illness are unknown. Loss-of-function (LoF) mutations in the gene encoding histone methyltransferase, SETD1A, confer substantial risk to schizophrenia. Among several roles, SETD1A is thought to be involved in the development and function of neuronal circuits. Here, we employed a multi-omics approach to study the effects of heterozygous Setd1a LoF on gene expression and synaptic composition in mouse cortex across five developmental timepoints from embryonic day 14 to postnatal day 70. Using RNA sequencing, we observed that Setd

SUBMITTER: Clifton NE 

PROVIDER: S-EPMC9476630 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature