ROS-based lethality of <i>Caenorhabditis elegans</i> mitochondrial electron transport mutants grown on <i>Escherichia coli</i> siderophore iron release mutants.

Abstract

<i>Caenorhabditis elegans</i> consumes bacteria, which can supply essential vitamins and cofactors, especially for mitochondrial functions that have a bacterial ancestry. Therefore, we screened the Keio <i>Escherichia coli</i> knockout library for mutations that induce the <i>C. elegans hsp-6</i> mitochondrial damage response gene, and identified 45 <i>E. coli</i> mutations that induce <i>hsp-6::gfp</i> We tested whether any of these <i>E. coli</i> mutations that stress the <i>C. elegans</i> mitochondrion genetically interact with <i>C. elegans</i> mutations in mitochondrial functions. Surprisingly, 4 <i>E. coli</i> mutations that disrupt the import or removal of iron from the bacterial siderophore enterobactin were lethal in combination with a collection of <i>C. elegans</i> mutations that disrupt particular iron-sulfur proteins of the electron transport chain. Bacterial mutations that fail to synthesize enterobactin are not synthetic lethal with these <i>C. elegans</i> mitochondrial mutants; it is the enterobactin-iron complex that is lethal in combination with the <i>C. elegans</i> mitochondrial mutations. Antioxidants suppress this inviability, suggesting that reactive oxygen species (ROS) are produced by the mutant mitochondria in combination with the bacterial enterobactin-iron complex.