Ferritins and iron accumulation in plant tissues

Abstract

At physiological pH, iron tends to precipitate as insoluble forms. Furthermore, its redox cycling participates in activation of reduced forms of oxygen through Fenton chemistry, leading to cellular damage and cell death. As a consequence of these properties, plants have evolved mechanisms to control iron uptake and storage. A class of multimeric proteins, the ferritins, acts as an iron buffer inside the cell by storing this ion in a soluble, non-toxic and bioavailable form. These proteins are present in plants, animals, fungi and bacteria. In plants, they are localized within plastids, and their synthesis is regulated by developmental and environmental factors, such as iron excess or oxidative stress. In particular, iron overload transcriptionally activates some ferritin genes. Both an abscissic acid-dependent and an abscissic acid-independent pathway are involved in this iron response. The latter involves some phosphorylation and dephosphorylation events, and specific cis-regulatory elements have been evidenced in some ferritin promoter sequences. Ferritin expression has been experimentally deregulated in transgenic plants by overexpressing them under the control of various heterologous promoters. As a consequence of ferritin accumulation in these transgenic plants, an increase in leaf or seed iron concentration by 2-to 3-fold was reported, concomitantly with an increase in root ferric reductase and root H+ -ATPase activities, two key determinants of iron uptake by dicotyledonous plants. This leads to propose a biotechnological approach to treat human iron deficiency estimated to affect 30% of the world population. However, the iron-enriched phenotype of plants over-Accumulating ferritins seems to be highly soil-type dependent. © 2006 Springer.