ENTEROBACTIN ROLES IN COPPER TOLERANCE AND TOXICITY

PERALTA DAIANA; BULACIO GIL NATALIA; FARIZANO JUAN V; CORBALÁN NATALIA S; POMARES M. FERNANDA; CARAM DI SANTO CAROLINA; RUBIO MOLINA CAROLINA; DE CRISTOBAL RICARDO; ZENOFF, ANA M; VINCENT PAULA A; ADLER CONRADO

VIRTUAL

Congreso; Reunión conjunta SAIB-SAMIGE; 2021

SAIB

The ability of siderophores to play roles beyond iron acquisition has been recently proven for many of them and evidence continues to grow. An earlier work showed that the siderophore enterobactin is able to increase copper toxicity by reducing Cu2+ to Cu+, which diffuses more easily across cell membranes. Copper toxicity is multifaceted and involves the formation of reactive oxygen species, mismetallation of enzymes and possibly other mechanisms. Given that we previously reported on the capacity of enterobactin to alleviate oxidative stress caused by various stressors other than copper, we considered the possibility that the siderophore could play a dual role regarding copper toxicity. In this work we found that the absence of enterobactin increased E. coli sensitivity to copper and that low concentrations of the siderophore had a protective effect by reducing reactive oxygen species (ROS). We also observed that copper induced the expression and production of the siderophore, counteracting the downregulation effect of iron. Interestingly, when we used enterobactin in high concentrations, cells became particularly sensitive to copper due to the Cu2+ to Cu+ reduction, which led to cell death.