Carbon Monoxide Modulates Auxin Transport and Nitric Oxide Signaling in Plants under Iron Deficiency Stress

Carbon monoxide (CO) and nitric oxide (NO) are signal molecules that enhance plant adaptation to environmental stimuli. Auxin is an essential phytohormone for plant growth and development. CO and NO play crucial roles in modulating the plant's response to iron deficiency. Iron deficiency leads to an increase in the activity of heme oxygenase (HO) and the subsequent generation of CO. Additionally, it alters the polar subcellular distribution of Pin-Formed 1 (PIN1) proteins, resulting in enhanced auxin transport. This alteration, in turn, leads to an increase in NO accumulation. Furthermore, iron deficiency enhances the activity of ferric chelate reductase (FCR), as well as the expression of the Fer-like iron deficiency-induced transcription factor 1 (FIT) and the ferric reduction oxidase 2 (FRO2) genes in plant roots. Overexpression of the long hypocotyl 1 (HY1) gene, which encodes heme oxygenase, or the CO donor treatment resulted in enhanced basipetal auxin transport, higher FCR activity, and the expression of FIT and FRO2 genes under Fe deficiency. Here, a potential mechanism is proposed: CO and NO interact with auxin to address iron deficiency stress. CO alters auxin transport, enhancing its accumulation in roots and up-regulating key iron-related genes like FRO2 and IRT1. Elevated auxin levels affect NO signaling, leading to greater sensitivity in root development. This interplay promotes FCR activity, which is crucial for iron absorption. Together, these molecules enhance iron uptake and root growth, revealing a novel aspect of plant physiology in adapting to environmental stress.