Intracellular iron sensing by the direct binding of iron to regulators
نویسندگان
چکیده
Iron (Fe) is an essential micronutrient for virtually all living organisms; it is incorporated into numerous proteins as Fe-sulfur (S) clusters, heme, or free Fe, and it mediates many metabolic processes, including photosynthesis and cellular respiration. Due to the low solubility and high reactivity of Fe, living cells must tightly regulate Fe acquisition in response to changes in Fe availability in the environment. The molecular components involved in Fe acquisition and its regulation have been studied extensively in plants, animals, fungi, and bacteria, revealing specific mechanisms in each kingdom. Fe acquisition in higher plants is mediated by a chelation-based pathway using mugineic acid family phytosiderophores (Strategy II) or a reduction-based pathway using ferric-chelate reductases (Strategy I), depending on the species (Römheld and Marschner, 1986). Molecular components involved in both pathways are induced under Fe deficiency and repressed under Fe sufficiency, primarily at the transcript level; however, protein-level regulation has also been reported for some components (Lan et al., 2011; Kobayashi and Nishizawa, 2012). To achieve expressional regulation based on Fe availability, Fe sensing systems must exist, but the signals and sensors have not been clarified in plants. Although various metabolites affected by Fe availability are thought to influence Fe deficiency responses, we propose that the direct binding of Fe to expressional regulators is the primary Fe sensing event in plant cells, similar to the mechanisms in animals, fungi, and bacteria. The recent identification of the Fe-binding regulators IDEF1 and HRZs/BTS in plants supports this hypothesis.
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