![]() ![]() coli strains and many other types of bacteria are harmless to humans, some are pathogenic, and these organisms also require iron, which they obtain from their host. In response, hosts have evolved several methods for depriving invading microorganisms of iron. 1 One such method is the synthesis of a protein known as lipocalin-2, which can sequester iron–siderophore complexes, thus making them unavailable to the bacteria. The battle for iron between the bacterium and its host can be summarized as follows: the microbe secretes siderophores to maximize its iron supply, while the host strives to keep its tenants in check by limiting that supply.Ī recent study by Qi and Han 2 reveals another layer of complexity to this relationship. They used a novel assay of microbial metabolites to examine their effects on the growth of the experimental roundworm Caenorhabditis elegans. They found that enterobactin produced by E. #SALT IRON WARS SERIES#Ĭoli was able to enhance the growth of the worm, and through a series of experiments they showed that the siderophore stimulates iron accumulation within the mitochondria of the worm’s cells. ![]() (The mitochondrion plays an important role in cellular iron homeostasis.) Interestingly, this accumulation was dependent on a mitochondrial enzyme, the α subunit of ATP synthase. ![]()
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