Stephen B. Watt

The paper combines natural and engineered genetic variation to identify 22 non-coding variants affecting haematological traits and shows how a CUX1 variant impacts megakaryopoiesis.

This study identifies genetic determinants of endothelial cell molecular traits and their overlap with disease GWAS loci, revealing shared and unique mechanisms in non-communicable diseases.

This study identifies 5,106 new genetic variants associated with blood cell traits using large-scale GWAS, highlighting the polygenic and monogenic basis of hematopoiesis.

This study uses regulatory QTLs from immune cells to fine-map causal variants for twelve immune-mediated diseases, finding smaller credible sets and higher posterior probabilities compared to traditional methods.

The paper identifies how variation in PU.1 binding and chromatin looping at neutrophil enhancers influences autoimmune disease susceptibility and cell count differences.

This study compares the epigenomes of neutrophils and monocytes to identify regulatory elements and chromatin states, revealing differences in enhancer activity and DNA methylation.

The paper measures and compares transcriptional and epigenetic variability across immune cell types and finds neutrophils exhibit higher variability linked to immune pathways and environmental exposure.