Marina Valenzuela-Villatoro

This study shows that loss of mitochondrial glutathione reductase and thioredoxin reductase in C. elegans causes growth, fertility, and muscle defects, activates a constitutive UPRmt, and alters mitochondrial morphology.

The paper shows that inactivating the NMD pathway suppresses the embryonic lethality of gsr-1 mutants in C. elegans by enabling the transsulfuration pathway to compensate for the loss of glutathione reductase function.