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A scalable model to dissect APOE-dependent mechanisms and identify therapeutic targets in AD is established, establishing a scalable model of disease pathogenesis and highlighting a central role for oxidized lipid metabolism in AD.
It is found that genetic repeatability is a common feature in the repeated evolution of cave traits, the extent of genetic repeatability varies across cave traits, and there is little evidence for widespread colocalization of sleep, eye loss, and metabolic traits within the genome.
The results reveal that recurrent deletion events have repeatedly contributed to the evolution of cave-adapted phenotypes and highlight deletions as underexplored contributors of adaptive evolution in a system characterized by trait loss.
Zebrafish is established as an efficient vertebrate platform for functional interrogation of GWAS candidates and an evolutionarily conserved cerebellar role for MEIS1 in sleep maintenance is supported, indicating conserved regulatory architecture spanning the human insomnia-associated locus.
Structural variants (SVs) are increasingly recognized as key contributors to adaptive evolution, yet they remain underexplored compared with single-nucleotide variation. To understand how large-scale genomic changes shape repeated evolution, we leveraged multiple levels of sequence data across the powerful evolutionary...
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