Saccharomyces cerevisiae (baker's yeast) is an excellent model for understanding fundamental biological mechanisms that are conserved in Nature and that have an impact on human disease. The metal iron is a redox-active cofactor that plays critical biochemical roles in a broad range of functions, including oxygen transport, mitochondrial oxidative phosphorylation, chromatin remodelling, intermediary metabolism and signalling. Although iron deficiency is the most common nutritional disorder on the planet, little is known about the metabolic adjustments that cells undergo in response to iron deficit and the regulatory mechanisms that allow these adaptive responses. In the present article, we summarize recent work on genome-wide metabolic reprogramming in response to iron deficiency, mediated by specific mRNA degradation mechanisms that allow S. cerevisiae cells to adapt to iron deficiency.
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