Molybdenum cofactor transfer from bacteria to nematode mediates sulfite detoxification.

Abstract

The kingdoms of life share many small molecule cofactors and coenzymes. Molybdenum cofactor (Moco) is synthesized by many archaea, bacteria, and eukaryotes, and is essential for human viability. The genome of the animal Caenorhabditis elegans contains all of the Moco biosynthesis genes, and surprisingly these genes are not essential if animals are fed a bacterial diet that synthesizes Moco. C. elegans lacking both endogenous Moco synthesis and dietary Moco from bacteria arrest development, demonstrating interkingdom Moco transfer. Our screen of E. coli mutants identified genes necessary for synthesis of bacterial Moco or transfer to C. elegans. Moco-deficient C. elegans developmental arrest is caused by loss of sulfite oxidase, a Moco-requiring enzyme, and is suppressed by mutations in either C. elegans cystathionine gamma-lyase or cysteine dioxygenase, blocking toxic sulfite production from cystathionine. Thus, we define the genetic pathways for an interkingdom dialogue focused on sulfur homeostasis.