Paul D. Goetsch

The paper presents a CURE model that identifies bacterial isolates producing bioactive metabolites antagonizing the C. elegans Ras signaling pathway through phenotype suppression.

This study shows that disrupting LIN-35-MuvB interaction in C. elegans impairs DREAM function but not chromatin localization, with limited target gene upregulation compared to LIN-35 loss.

This paper shows that Drosophila Myb can bind to nematode LIN9 and LIN52 proteins and cause a synthetic multivulval phenotype in C. elegans, despite their distant evolutionary divergence.