<i>Rhizobium</i> induces DNA damage in <i>Caenorhabditis elegans</i> intestinal cells.

Abstract

In their natural habitat of rotting fruit, the nematode <i>Caenorhabditis elegans</i> feeds on the complex bacterial communities that thrive in this rich growth medium. Hundreds of diverse bacterial strains cultured from such rotting fruit allow <i>C. elegans</i> growth and reproduction when tested individually. In screens for <i>C. elegans</i> responses to single bacterial strains associated with nematodes in fruit, we found that <i>Rhizobium</i> causes a genome instability phenotype; we observed abnormally long or fragmented intestinal nuclei due to aberrant nuclear division, or defective karyokinesis. The karyokinesis defects were restricted to intestinal cells and required close proximity between bacteria and the worm. A genetic screen for <i>C. elegans</i> mutations that cause the same intestinal karyokinesis defect followed by genome sequencing of the isolated mutant strains identified mutations that disrupt DNA damage repair pathways, suggesting that <i>Rhizobium</i> may cause DNA damage in <i>C. elegans</i> intestinal cells. We hypothesized that such DNA damage is caused by reactive oxygen species produced by <i>Rhizobium</i> and found that hydrogen peroxide added to benign <i>Escherichia coli</i> can cause the same intestinal karyokinesis defects in WT <i>C. elegans</i> Supporting this model, free radical scavengers suppressed the <i>Rhizobium</i>-induced <i>C. elegans</i> DNA damage. Thus, <i>Rhizobium</i> may signal to eukaryotic hosts via reactive oxygen species, and the host may respond with DNA damage repair pathways.