RT Journal Article
SR Electronic
T1 Interkingdom competition for Fe(III) revealed by a synthetic lethal interaction between <em>Caenorhabditis elegans</em> mitochondrial electron transport and <em>Escherichia coli</em> siderophore iron release mutations
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 707968
DO 10.1101/707968
A1 J. Amaranath Govindan
A1 Elamparithi Jayamani
A1 Gary Ruvkun
YR 2019
UL http://biorxiv.org/content/early/2019/07/19/707968.abstract
AB C. elegans consumes bacteria which can supply essential vitamins and cofactors especially for mitochondrial functions ancestrally related to bacteria. Therefore, we screened the Keio E. coli knockout library for mutations that induce a C. elegans mitochondrial damage response gene. We identified 45 E. coli mutations that induce a the C. elegans hsp-6::gfp response gene. Surprisingly, four of these E. coli mutations that disrupt the import or removal of iron from the bacterial siderophore enterobactin were lethal in combination with C. elegans 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 C. elegans mitochondrial mutants; it is the enterobactin-iron complex that is lethal in combination with the C. elegans 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.