Fullerenol affects maize plants depending on their iron status

Iron (Fe) is essential for plants as a co-factor of enzymes of key metabolic processes including respiration and photosynthesis (Marschner 1995). Iron is an element abundant in the earth’s crust. However, at high pH and high bicarbonate content of calcareous soils, the availability of Fe to plants is often reduced. The deficiency of bioavailable Fe leads to a characteristic chlorotic phenotype that begins to develop in the youngest leaves. Iron deficiency chlorosis is a common nutritional disorder affecting plants and one of the major limiting factors for crop production in many areas of the world (Vose 1982, Alloway 2008). To maintain Fe homeostasis, plants have evolved mechanisms to acquire Fe under conditions of limited availability. Maize, like other Fe-deficient grasses, respond to Fe deficiency through the so-called Strategy II, which includes 1) the release of phytosiderophores (PSs) for chelate FeIII (ferric) ions in soil and 2) the induction of a transporter specific for FeIII-PS complex in the root cell plasma membrane (Römheld and Marschner 1986). Plant PSs belong to the mugineic acid (MA) family of chelators (Hell and Stephan 2003). Both reactions of this chelationbased strategy enhanced in response to Fe deficiency are directed to improve Fe uptake. In maize, the Yellow Stripe 1 (YS1) gene encoding FeIII-PS transporter was firstly identified by Curie et al. (2001). It has been suggested that the maize YS1 (ZmYS1) is involved in both primary Fe acquisition and intracellular transport of Fe and other metals