| Literature DB >> 34416157 |
Nil Aygün1, Angela L Elwell1, Dan Liang1, Michael J Lafferty1, Kerry E Cheek1, Kenan P Courtney1, Jessica Mory1, Ellie Hadden-Ford1, Oleh Krupa1, Luis de la Torre-Ubieta2, Daniel H Geschwind2, Michael I Love3, Jason L Stein4.
Abstract
Interpretation of the function of non-coding risk loci for neuropsychiatric disorders and brain-relevant traits via gene expression and alternative splicing quantitative trait locus (e/sQTL) analyses is generally performed in bulk post-mortem adult tissue. However, genetic risk loci are enriched in regulatory elements active during neocortical differentiation, and regulatory effects of risk variants may be masked by heterogeneity in bulk tissue. Here, we map e/sQTLs, and allele-specific expression in cultured cells representing two major developmental stages, primary human neural progenitors (n = 85) and their sorted neuronal progeny (n = 74), identifying numerous loci not detected in either bulk developing cortical wall or adult cortex. Using colocalization and genetic imputation via transcriptome-wide association, we uncover cell-type-specific regulatory mechanisms underlying risk for brain-relevant traits that are active during neocortical differentiation. Specifically, we identified a progenitor-specific eQTL for CENPW co-localized with common variant associations for cortical surface area and educational attainment.Entities:
Keywords: cell-type specificity; common genetic variants; expression/splicing quantitative loci; genome-wide association study; neurogenesis; neuropsychiatric disorders; transcriptome-wide association study
Mesh:
Substances:
Year: 2021 PMID: 34416157 PMCID: PMC8456186 DOI: 10.1016/j.ajhg.2021.07.011
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.043