Plant hormones influencing iron uptake in plants

Abstract

Different experimental results based on split-root and grafting experiments suggest the involvement of systemic signals in the regulation of Fe deficiency stress responses by Strategy I plants. Until now, the nature of this (or these) systemic signal(s) is unknown, but several authors have proposed some plant hormones, or their precursors, as participants in this signalling process. Among the hormones that have received more attention are auxin and ethylene. Both of them can induce morphological changes similar to the ones induced by Fe deficiency, such as subapical root hairs and transfer cells, when applied to Fe-sufficient Strategy I plants. Furthermore, the addition of either auxin or ethylene inhibitors to Fe-deficient Strategy I plants can block some of these morphological changes. These results, and others obtained by using ethylene mutants and other experimental approaches, suggest that auxin and/or ethylene could be involved in the regulation of some of the morphological changes developed by Fe-deficient Strategy I plants. Since auxin can increase the production of ethylene, some of the effects of auxin could be mediated through ethylene. Auxin and ethylene have also been involved in the regulation of some of the physiological responses to Fe deficiency developed by Strategy I plants, such as acidification and ferric reductase activity. However, their participation in such regulation is more controversial. There are no studies relating hormones to Fe uptake in Strategy II plants, although ethylene and phytosiderophores share common precursors. Auxin and ethylene have also been involved in other nutrient deficiencies, namely those of P and K. In this chapter, we review existing evidence suggesting a role for auxin, ethylene and other hormones and signaling substances in the regulation of Fe deficiency stress responses and other aspects of Fe nutrition, and discuss the involvement of hormones in the responses to other nutrient deficiencies. © 2006 Springer.