Knock-out of ferritin AtFerl causes earlier onset of age-dependent leaf senescence in Arabidopsis

Ferritins are iron-storage proteins involved in the regulation of free iron levels in the cells. Arabidopsis thaliana AtFerl ferritin, one of the best characterized plant ferritin isoforms to date, strongly accumulates upon treatment with excess iron, via a nitric oxide-mediated pathway. However other environmental factors, such as exposure to oxidative stress or to pathogen attack, as well as developmental factors regulate AtFerl transcript levels. In particular, recent findings have highlighted an accumulation of the ferritin transcript during senescence. To investigate the physiological relevance of AtFerl ferritin during senescence we isolated an Arabidopsis mutant knock-out in the AtFerl gene, which we named atferl-2. We analyzed it together with a second, independent AtFerl KO mutant, the atferl-l mutant. Interestingly, both atferl-1 and atferl-2 mutants show symptoms of accelerated natural senescence; the precocious leaf yellowing is accompanied by accelerated decrease of maximal photochemical efficiency and chlorophyll degradation. However, no accelerated senescence upon dark treatment was observed in the atferl mutants with respect to their wt. These results suggest that AtFerl ferritin isoform is functionally involved in events leading to the onset of age-dependent senescence in Arabidopsis and that its iron-detoxification function during senescence is required when reactive oxygen species accumulate. (C) 2007 Elsevier Masson SAS. All rights reserved.