Physiological and molecular mechanisms of plant-root responses to iron toxicity

Copyright © 2024 Elsevier GmbH. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Journal of plant physiology. - 1979. - 297(2024) vom: 20. Juni, Seite 154257
1. Verfasser: Li, Guangjie (VerfasserIn)
Weitere Verfasser: Wu, Jinlin, Kronzucker, Herbert J, Li, Baohai, Shi, Weiming
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:Journal of plant physiology
Schlagworte:Journal Article Review Iron toxicity Molecular mechanisms Response Roots Signaling
Beschreibung
Zusammenfassung:Copyright © 2024 Elsevier GmbH. All rights reserved.
The chemical form and physiological activity of iron (Fe) in soil are dependent on soil pH and redox potential (Eh), and Fe levels in soils are frequently elevated to the point of causing Fe toxicity in plants, with inhibition of normal physiological activities and of growth and development. In this review, we describe how iron toxicity triggers important physiological changes, including nitric-oxide (NO)-mediated potassium (K+) efflux at the tips of roots and accumulation of reactive oxygen species (ROS) and reactive nitrogen (RNS) in roots, resulting in physiological stress. We focus on the root system, as the first point of contact with Fe in soil, and describe the key processes engaged in Fe transport, distribution, binding, and other mechanisms that are drawn upon to defend against high-Fe stress. We describe the root-system regulation of key physiological processes and of morphological development through signaling substances such as ethylene, auxin, reactive oxygen species, and nitric oxide, and discuss gene-expression responses under high Fe. We especially focus on studies on the physiological and molecular mechanisms in rice and Arabidopsis under high Fe, hoping to provide a valuable theoretical basis for improving the ability of crop roots to adapt to soil Fe toxicity
Beschreibung:Date Completed 19.05.2024
Date Revised 20.06.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1618-1328
DOI:10.1016/j.jplph.2024.154257