Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.

Osteoarthritis (OA) poses a significant healthcare burden with limited treatment options. While genome-wide association studies (GWASs) have identified over 100 OA-associated loci, translating these findings into therapeutic targets remains challenging. To address this gap, we mapped gene expression, chromatin accessibility, and 3D chromatin structure in primary human articular chondrocytes in both resting and OA-mimicking conditions.

Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.

Osteoarthritis (OA) poses a significant healthcare burden with limited treatment options. While genome-wide association studies (GWAS) have identified over 100 OA-associated loci, translating these findings into therapeutic targets remains challenging. Integrating expression quantitative trait loci (eQTL), 3D chromatin structure, and other genomic approaches with OA GWAS data offers a promising approach to elucidate disease mechanisms; however, comprehensive eQTL maps in OA-relevant tissues and conditions remain scarce.

Recent progress in understanding the genomic architecture of sexual conflict.

Genomic conflict between the sexes over shared traits is widely assumed to be resolved through the evolution of sex-biased expression and the subsequent emergence of sexually dimorphic phenotypes. However, while there is support for a broad relationship between genome-wide patterns of expression level and sexual conflict, recent studies suggest that sex differences in the nature and strength of interactions between loci are instead key to conflict resolution. Furthermore, the advent of new technologies for measuring and perturbing expression means we now have much more power to detect genomic signatures of sexual conflict.