Molecular mechanisms of resistance to human pathogenic bacteria in Caenorhabditis elegans by MEV-1 mediated oxidative stress.

Both mutation and knockdown in mev-1 gene render Caenorhabditis elegans susceptibility to Enterococcus faecalis infection. However, the mechanisms by which of MEV-1 defects pathogen resistance remain unclear. Here we show that mev-1RNAi causes a dramatic decrease in oxidative stress and antioxidant enzyme expressions, thereby leading to increased E. faecalis accumulation in nematode intestine. Mitochondrial superoxide change after infection induced these oxidative responses through DAF-16 activity. All together, this highlights MEV-1 as a key regulatory component for determining genetic responsiveness to oxidant/antioxidant imbalance that is associated with innate immunity.