NITRIC OXIDE MEDIATES IRON INDUCTION OF FERRITIN ACCUMULATION IN ARABIDOPSIS THALIANA

Nitric oxide (NO) is a signaling molecule involved in many different functions in mammal cells, among which the regulation of iron homeostasis. The recent discovery of NO-mediated regulation of aconitase activity also in plant cells prompted us to investigate the possible role of NO as regulator of iron homeostasis in plant cells, in particular its involvement in the regulation of A.thaliana ferritin, an iron-storage protein which accumulates in response to iron increase. The infiltration of the NO-donor SNP in Arabidopsis leaves caused a sustained accumulation of the transcript encoding ferritin; protein accumulation was also observed, although at much lower extent. The NO-dependent accumulation of ferritin transcript was observed also in iron-depleted Arabidopsis cells, whereas CPTIO, a NO scavenger, was able to completely abolish ferritin transcript accumulation caused by iron loading. To establish a possible involvement of cGMP as signal in in NO-mediated ferritin accumulation, we treated cells with 8 Br-cGMP, a cGMP analogous able to permeate cells. 8Br-cGMP was not sufficient to either induce ferritin accumulation nor to act synergistically with iron or SNP cGMP was not even found to participate to this signalling pathway since ODQ, an inhibitor of NO-dependent guanilate cyclase was not able to repress iron- nor SNP-induced ferritin accumulation. Furthermore calyculin, a Ser/Thr phosphatase inhibitor, completely abolished iron- or SNP-induced transcript accumulation. We propose that NO locates downstream of iron in the signalling pathway leading to ferritin accumulation which proceeds, beyond NO, through cGMP independent, Ser/Thr phosphatase dependent steps.