Excess iron stress reduces root tip zone growth through nitric oxide‐mediated repression of potassium homeostasis in Arabidopsis
Excess iron stress reduces root tip zone growth through nitric oxide‐mediated repression of potassium homeostasis in Arabidopsis
Summary The root tip zone is regarded as the principal action site for iron (Fe) toxicity and is more sensitive than other root zones, but the mechanism underpinning this remains largely unknown. We explored the mechanism underpinning the higher sensitivity at the Arabidopsis root tip and elucidated the role of nitric oxide (NO) using NO‐related mutants and pharmacological methods. Higher Fe sensitivity of the root tip is associated with reduced potassium (K+) retention. NO in root tips is increased significantly above levels elsewhere in the root and is involved in the arrest of primary root tip zone growth under excess Fe, at least in part related to NO‐induced K+ loss via SNO1 (sensitive to nitric oxide 1)/SOS4 (salt overly sensitive 4) and reduced root tip zone cell viability. Moreover, ethylene can antagonize excess Fe‐inhibited root growth and K+ efflux, in part by the control of root tip NO levels. We conclude that excess Fe attenuates root growth by effecting an increase in root tip zone NO, and that this attenuation is related to NO‐mediated alterations in K+ homeostasis, partly via SNO1/SOS4.
- State Key Laboratory of Soil and Sustainable Agriculture China (People's Republic of)
- University of Melbourne Australia
- University of Chinese Academy of Sciences China (People's Republic of)
- Chinese Academy of Sciences China (People's Republic of)
- Institute of Soil Science China (People's Republic of)
580, 570, Cell Death, Arabidopsis Proteins, Iron, Arabidopsis, Ethylenes, Nitric Oxide, Plants, Genetically Modified, Plant Roots, Stress, Physiological, Potassium, Homeostasis, Pyridoxal Kinase
580, 570, Cell Death, Arabidopsis Proteins, Iron, Arabidopsis, Ethylenes, Nitric Oxide, Plants, Genetically Modified, Plant Roots, Stress, Physiological, Potassium, Homeostasis, Pyridoxal Kinase
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