Research articleNitric oxide signaling is involved in the response to iron deficiency in the woody plant Malus xiaojinensis

- Malus xiaojenensis alters its root morphology and physiology under Fe deficiency.
- Treatment with a NO scavenger blocks the Fe deficiency root phenotype.
- Treatment with a NO donor restores the Fe deficiency root phenotype.
- NO is thus an important mediator of responses to Fe deficiency in M. xiaojinensis.

To cope with iron (Fe) deficiency, plants have evolved a wide range of adaptive responses from changes in morphology to altered physiological responses. Recent studies have demonstrated that nitric oxide (NO) is involved in the Fe-deficiency response through hormonal signaling pathways. Here, we report that NO plays a significant role in Malus xiaojinensis, an Fe-efficient woody plant. Fe deficiency triggered significant accumulation of NO in the root system, predominantly in the outer cortical and epidermal cells of the elongation zone. The NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (cPTIO) completely arrested Fe deficiency-induced root hair formation, blocked the increase in root ferric-chelate reductase activity and in root H+ excretion, further reduced the active iron content in young leaves and roots, and prevented the upregulation of the critical Fe-related genes, FIT, MxFRO2-like, and MxIRT1. These conditions were restored under Fe deficiency by treatment with the NO donor, sodium nitroprusside (SNP). Additionally, chlorophyll content and relative expression levels of the genes chlorophyll a deoxygenase (MxCAO) and polyamine oxidase (MxPAO) were not changed significantly following Fe deficiency for 6 d; however, SNP treatment increased MxHEMA gene expression. Interestingly, the Fv/Fm ratio, the maximum quantum yield of photosystem II (PSII), decreased significantly following cPTIO treatment. We observed more severe chlorosis under Fe deficiency with cPTIO treatment for 9 d. These results strongly suggest that NO mediates a range of responses to Fe deficiency in M. xiaojinensis, from morphological changes to the regulation of physiological processes and gene expression.

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