Genome-wide association analyses of magnetic resonance imaging data describe the genetic architecture of 13 cortical phenotypes at both global and regional levels, implicating neurodevelopmental and constrained genes.

Tissue co-regulation score regression (TCSC) infers causal tissues and partitions trait heritability into tissue-specific components using a transcriptome-wide association study framework. Applying TCSC to 78 complex traits and diseases identifies biologically plausible tissue–trait relationships.

Single-cell multi-omic analyses show that chronic inflammation contributes to myeloproliferative neoplasm transformation to secondary acute myeloid leukemia by enhancing tumor protein 53 (TP53) mutant cell fitness and genetic evolution.

High-quality genome assemblies of four Solanum Americanum accessions lead to the identification of three NLR-encoding genes, Rpi-amr4, R02860 and R04373, that recognize potato late blight pathogen Phytophthora infestans effectors.

Analysis of H3K27ac genome-wide maps across 387 brain, heart, muscle and lung samples, along with eQTL and genome-wide association studies (GWAS) data integration, identifies tissue-specific genetically influenced active regulatory regions and target genes that potentially mediate disease etiology.

Multi-omic analysis of 579 patients with hormone receptor-positive (HR⁺)/human epidermal growth factor receptor 2-negative (HER2⁻) breast cancer identifies subgroups of the disease with distinct biological and clinical features.

Multi-ancestry genome-wide association meta-analysis identifies new risk loci for CAC. Functional evidence implicates candidate causal genes as regulators of smooth muscle cell-mediated calcification.

CT-SLEB, a powerful and scalable method, improves the performance of multiancestry polygenic prediction by generating polygenic risk scores based on GWAS summary statistics in diverse populations.

Gain-of-function perturbation screens across 488 barcoded cell lines identify context-specific activation lethalities. The authors show that cells with MAPK, PI3K and WNT pathway activation are vulnerable to mutations that lead to further activation, suggesting a new strategy for treating tumors driven by these oncogenic pathways.

Genetic fine-mapping and CRISPRi screens identify functional variants and their target genes associated with Alzheimer’s disease in microglia. The variant rs7922621 modulates AD risk through control of TSPAN14 expression in this cell type.