Nature Genetics

Cumulative transcription factor binding and p300-mediated histone acetylation drive enhancer activation frequency

Valentina Baderna — 2026-07-31

Nature Genetics, Published online: 31 July 2026; doi:10.1038/s41588-026-02703-x

This study uses single-molecule footprinting to quantify chromatin accessibility at enhancers and promoters in mouse embryonic stem cells and to dissect the contributions of transcription factor binding and chromatin context.

Gene mutant dosage is associated with prognosis and metastatic tropism in 60,000 clinical cancer samples

Nicola Calonaci — 2026-07-31

Nature Genetics, Published online: 31 July 2026; doi:10.1038/s41588-026-02666-z

The authors present INCOMMON, an open-source Bayesian inference tool that determines the multiplicity and copy number of driver mutations from tumor sequencing datasets.

Mediators of cell fate decisions in human fetal kidney development identified using spatial transcriptomics

2026-07-30

Nature Genetics, Published online: 30 July 2026; doi:10.1038/s41588-026-02679-8

During human development, the human kidney reproducibly generates approximately one million patterned nephrons. Using spatial transcriptomics and functional validation studies, we help identify how ligands and cell–cell interactions coordinate this complex process.

Single-cell spatial mapping of human kidney development implicates the microenvironment in guiding cell fate decisions

Jonathan Levinsohn — 2026-07-30

Nature Genetics, Published online: 30 July 2026; doi:10.1038/s41588-026-02665-0

The spatial organization of human kidney development is explored using single-cell RNA sequencing and spatial transcriptomics, highlighting the crucial role of microenvironmental signals in guiding cell fate.

Inflammatory bowel disease and cancer-driving mutations occupy different cellular neighborhoods

2026-07-29

Nature Genetics, Published online: 29 July 2026; doi:10.1038/s41588-026-02686-9

With the profound epithelial and stromal remodeling observed in inflammatory bowel disease, why does progression to cancer often take decades? Using a mouse model of early malignant lesions arising from colitis, we identify a close link between tissue repair and neoplasia, whereas immune-refractory cellular neighborhoods appear relatively protected.

Translating genomic data into healthcare practice with the Singapore National Precision Medicine program

Shih Wee Seow — 2026-07-29

Nature Genetics, Published online: 29 July 2026; doi:10.1038/s41588-026-02687-8

Singapore’s National Precision Medicine program phase II establishes a multi-ancestry Asian population cohort, national-scale genetic testing and public–private partnerships, demonstrating how small countries can contribute to global genomics efforts.

Multi-ancestry genome-wide association analyses provide insights into the genetic basis of Hashimoto’s thyroiditis

Melissa N. Bujnis — 2026-07-29

Nature Genetics, Published online: 29 July 2026; doi:10.1038/s41588-026-02704-w

Multi-ancestry genome-wide association analyses of Hashimoto’s thyroiditis identify new risk loci and highlight shared genetic architecture with other autoimmune diseases and pleiotropic effects on clinical outcomes.

Paired mutation calling and spatial transcriptomics identify cellular neighborhoods associated with the neoplastic outcome of mouse colitis

Elisa B. Moutin — 2026-07-28

Nature Genetics, Published online: 28 July 2026; doi:10.1038/s41588-026-02673-0

This study uses a mouse model of inflammatory bowel disease to explore how mutations and cellular context combine to drive the transition to malignancy.