Using genetic buffering relationships identified in fission yeast to reveal susceptibilities in cells lacking hamartin or tuberin function.

Tuberous sclerosis complex is an autosomal dominant disorder characterized by benign tumors arising from the abnormal activation of mTOR signaling in cells lacking TSC1 (hamartin) or TSC2 (tuberin) activity. To expand the genetic framework surrounding this group of growth regulators, we utilized the model eukaryote to uncover and characterize genes that buffer the phenotypic effects of mutations in the orthologous or loci. Our study identified two genes: (encoding a DNA helicase) and (encoding a peptidyle-prolyl cis/trans isomerase).