Transcriptome analysis identifies an ASD-Like phenotype in oligodendrocytes and microglia from C58/J amygdala that is dependent on sex and sociability.
George D DaltonStephen K SiecinskiViktoriya D NikolovaGary P CoferKathryn J HornburgYi QiG Allan JohnsonYong-Hui JiangSheryl S MoySimon G GregoryPublished in: Behavioral and brain functions : BBF (2024)
Our work demonstrates the C58/J mouse model's utility in evaluating the influence of sex and sociability on the transcriptome in concomitant brain regions involved in ASD. Our single-nucleus transcriptome analysis elucidates potential pathological roles of oligodendrocytes and microglia in ASD. This investigation provides details regarding regulatory features disrupted in these cell types, including transcriptional gene dysregulation, aberrant cell differentiation, altered gene regulatory networks, and changes to key pathways that promote microglia/oligodendrocyte differentiation. Our studies provide insight into interactions between genetic risk and epigenetic processes associated with divergent affiliative behavior and lack of positive sociability.
Keyphrases
- autism spectrum disorder
- genome wide
- resting state
- inflammatory response
- dna methylation
- mouse model
- attention deficit hyperactivity disorder
- functional connectivity
- gene expression
- neuropathic pain
- single cell
- intellectual disability
- copy number
- transcription factor
- rna seq
- cell therapy
- spinal cord
- spinal cord injury
- mesenchymal stem cells
- stem cells
- cerebral ischemia
- subarachnoid hemorrhage
- genome wide identification
- heat shock
- risk assessment
- climate change