This study addresses the question of the interference between Fe nutrition and Cd toxicity at the level
of growth performance, phytosiderophores (PS) release, micronutrient accumulation and expression
of genes involved in Fe homeostasis in barley seedlings, a plant with Strategy II-based response to Fe
shortage. Cd exposure induced responses similar to those of genuine Fe deficiency also in Fesufficient
plants. Most genes involved in PS biosynthesis and secretion (HvNAS3, HvNAS4, HvNAS6,
HvNAS7, HvNAAT-A, HvDMAS1 and HvTOM1) induced by Fe deprivation were also significantly upregulated
in presence of Cd under Fe sufficient conditions. Accordingly, the enhanced expression of
these genes in roots under Cd exposure was accompanied by an increase of PS release. However,
induced expression of HvIRO2 and the down-regulation of HvIDEF1 and HvIRT1, after Cd exposure,
suggested the presence of a pathway that induces HvIRO2-mediated PS biosynthesis under Cd stress,
which probably is not simply caused by Fe deficiency. The down-regulation of HvIRT1 and
HvNramp5 may represent a protective mechanism at transcriptional level against further Cd uptake by
these transporters. These results likely indicate that Cd itself may be able to activate Fe acquisition
mechanism in an Fe-independent manner.
