Iron (Fe) deficiency is a widespread
nutritional disorder on calcareous
soils. To identify genes involved in the Fe deficiency response, Arabidopsis (Arabidopsis thaliana) transfer
DNA insertion lines were screened on a high-pH medium with low Fe availability. This approach identified
METAL TOLERANCE PROTEIN8 (MTP8), a member of the
Cation Diffusion Facilitator family, as a critical determinant for the tolerance to Fe deficiency-induced
chlorosis, also on soil substrate. Subcellular localization to the tonoplast, complementation of a
manganese (Mn)-sensitive Saccharomyces cerevisiae yeast strain, and Mn sensitivity of mtp8 knockout mutants characterized the
protein as a vacuolar Mn transporter suitable to prevent plant cells from Mn toxicity. MTP8 expression was strongly induced on low-Fe as well as high-Mn medium, which were both strictly dependent on the
transcription factor FIT, indicating that high-Mn stress induces Fe deficiency. mtp8 mutants were only hypersensitive to Fe deficiency when Mn was present in the medium, which further suggested an Mn-specific role of MTP8 during Fe limitation. Under those conditions, mtp8 mutants not only translocated more Mn to the shoot than did wild-type plants but suffered in particular from critically low Fe concentrations and, hence, Fe
chlorosis, although the transcriptional Fe deficiency response was up-regulated more strongly in mtp8. The diminished uptake of Fe from Mn-containing low-Fe medium by mtp8 mutants was caused by an impaired ability to boost the
ferric chelate reductase activity, which is an essential process in Fe acquisition. These findings provide a mechanistic explanation for the long-known interference of Mn in Fe nutrition and define the molecular processes by which plants alleviate this antagonism.