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Together, these results implicate a constellation of rare variants that map onto neuronal biology and demonstrate that diverse global populations converge on shared genetic signals underlying BD risk.
This study establishes large-scale adipocyte cell villages as a powerful and generalizable framework to map the context-dependent regulatory architecture of cardiometabolic disease and provides a resource linking human genetic variation to adipocyte cellular programs.
In adipose-derived mesenchymal stem cells exposed to metabolic stimulations, CASTIE increased eGene discovery by 36-92% across cell populations and identified stimulation-dependent regulatory effects at metabolic trait loci, revealing disease-relevant regulatory variation beyond static eQTL mapping.
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