Human-lineage-specific genomic elements are associated with neurodegenerative disease and APOE transcript usage.
Zhongbo ChenDavid ZhangRegina Hertfelder ReynoldsEmil Karl GustavssonSonia García-RuizKarishma D'SaAine Fairbrother-BrowneJana Vandrovcovanull nullJohn HardyHenry HouldenSarah A Gagliano TaliunJuan BotíaMina RytenPublished in: Nature communications (2021)
Knowledge of genomic features specific to the human lineage may provide insights into brain-related diseases. We leverage high-depth whole genome sequencing data to generate a combined annotation identifying regions simultaneously depleted for genetic variation (constrained regions) and poorly conserved across primates. We propose that these constrained, non-conserved regions (CNCRs) have been subject to human-specific purifying selection and are enriched for brain-specific elements. We find that CNCRs are depleted from protein-coding genes but enriched within lncRNAs. We demonstrate that per-SNP heritability of a range of brain-relevant phenotypes are enriched within CNCRs. We find that genes implicated in neurological diseases have high CNCR density, including APOE, highlighting an unannotated intron-3 retention event. Using human brain RNA-sequencing data, we show the intron-3-retaining transcript to be more abundant in Alzheimer's disease with more severe tau and amyloid pathological burden. Thus, we demonstrate potential association of human-lineage-specific sequences in brain development and neurological disease.
Keyphrases
- endothelial cells
- white matter
- induced pluripotent stem cells
- single cell
- cognitive decline
- resting state
- pluripotent stem cells
- transcription factor
- rna seq
- genome wide
- type diabetes
- big data
- gene expression
- multiple sclerosis
- adipose tissue
- machine learning
- metabolic syndrome
- risk assessment
- risk factors
- small molecule
- skeletal muscle
- cell fate
- cerebrospinal fluid
- binding protein
- drug induced
- amino acid