Kevin R. Roy

The paper shows that the m6A writer spares canonical 3' splice sites from methylation, allowing efficient splicing despite cotranscriptional methylation.

The paper develops a CRISPR-based platform to scan mutations in essential genes, applying it to Nrd1 to identify critical residues in its CTD-interacting domain.

The paper identifies gene-perturbation interactions across genetic backgrounds in yeast using CRISPRi and combinatorial DNA barcode sequencing, revealing 460 genes with variable effects and 234 interacting loci.

The paper develops MAGESTIC 3.0, a CRISPR-based system for genome-wide variant installation in yeast, revealing missense variants and multiple causal variants in quantitative trait loci across environmental conditions.

This study shows that inactivating Prp18p leads to global activation of alternative 3' splice sites with divergent sequences, without affecting cellular fitness.

The paper shows that in diploids, epistasis frequently modifies both additivity and dominance.

The paper identifies a recurrent tumor-specific transcript fusion between CDKN1A and RAB44 caused by splice-site mutations and shows its correlation with TP53 inactivation and CDK activation.