Zinc is essential, but toxic in excess, so bacteria modulate expression of pumps that either import or export zinc. They can also change their requirements by altering the zinc content of ribosomes. To investigate whether bacteria have other mechanisms for coping with zinc deficiency, Mark Paget of the University of Sussex, Brighton, United Kingdom, et al. knocked out the key regulator Zur in the antibiotic-producing bacterium Streptomyces coelicolor. "To our surprise, a previously silent large secondary metabolic gene cluster was switched on," says Paget. "This cluster directs the production of coelibactin, which is predicted to be a siderophore-related non-ribosomally-encoded peptide. Siderophores by definition bind iron, yet this finding suggests that coelibactin might actually be a zinc chelator. There is a growing interest in zinc chelation because zinc is thought to accelerate the formation of fibrillar beta-amyloid in Alzheimer's patients, and specific chelators are already undergoing clinical trials. Characterization of natural zincophores might provide a further route to therapies."

(D. Kallifidas, B. Pascoe, G. A. Owen, C. M. Strain-Damerell, H. J. Hong, and M. S. B. Paget. 2010. The zinc-responsive regulator Zur controls expression of the coelibactin gene cluster in Streptomyces coelicolor. J. Bacteriol. 192:608-611.)