Knocking out of the mitochondrial AtFer4 ferritin does not alter response of Arabidopsis plants to abiotic stresses.

Ferritins are iron-storage proteins which, in Arabidopsis, have a clear role in protection against oxidative stress. Plant ferritins are localized mainly in chloroplasts, but they can also be targeted to mitochondria; the ATFER4 ferritin isoform, according to bioinformatic subcellular predictors, has the highest scores for such localization in Arabidopsis. We isolated atfer4-2 mutant KO in the AtFer4 gene and we characterized it together with a second, independent mutant atfer4-1. We show that ATFER4 is indeed localized in mitochondria of Fe-treated Arabidopsis plants; when grown under Fe excess, atfer4 plants manifest, however, the same toxicity symptoms and O(2) consumption rates as wt plants. No enhanced sensitivity to oxidative conditions was observed in atfer4 seedlings exposed to salinity, osmotic stress, cold stress or oxidative stress elicited by paraquat. The growth response of roots and aerial parts in atfer4 plants under different light conditions was the same as wt. Also, the process of natural senescence, in which AtFer1 takes active part, was not perturbed in atfer4 plants. We conclude that the ATFER4 ferritin role in counteracting the environmental or developmental oxidative conditions in Arabidopsis plants is ancillary to that of the other isoforms, regardless of its mitochondrial localization. Copyright 2009 Elsevier GmbH. All rights reserved.