Ammonium nutrition modifies cellular calcium distribution influencing ammonium-induced growth inhibition
Copyright © 2024 Elsevier GmbH. All rights reserved.
Veröffentlicht in: | Journal of plant physiology. - 1979. - 298(2024) vom: 15. Juni, Seite 154264 |
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1. Verfasser: | |
Weitere Verfasser: | , , , , , |
Format: | Online-Aufsatz |
Sprache: | English |
Veröffentlicht: |
2024
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Zugriff auf das übergeordnete Werk: | Journal of plant physiology |
Schlagworte: | Journal Article Ammonium stress Ca(2+) homeostasis Cell wall properties Cellular Ca(2+) localization Ammonium Compounds Calcium SY7Q814VUP |
Zusammenfassung: | Copyright © 2024 Elsevier GmbH. All rights reserved. Proper plant growth requires balanced nutrient levels. In this study, we analyzed the relationship between ammonium (NH4+) nutrition and calcium (Ca2+) homeostasis in the leaf tissues of wild-type and mutant Arabidopsis specimens provided with different nitrogen sources (NH4+ and nitrate, NO3-). Providing plants with NH4+ as the sole nitrogen source disrupts Ca2+ homeostasis, which is essential for activating signaling pathways and maintaining the cell wall structure. The results revealed that the lower Ca2+ content in Arabidopsis leaves under NH4+ stress might result from reduced transpiration pull, which could impair root-to-shoot Ca2+ transport. Moreover, NH4+ nutrition increased the expression of genes encoding proteins responsible for exporting Ca2+ from the cytosol of leaf cells. Furthermore, overexpression of the Ca2+/H+ antiporter 1 (CAX1) gene alleviates the effects of NH4+ syndrome, including stunted growth. The oeCAX1 plants, characterized by a lower apoplastic Ca2+ level, grew better under NH4+ stress than wild-type plants. Evaluation of the mechanical properties of the leaf blades, including stiffness, strength, toughness, and extensibility, showed that the wild-type and oeCAX1 plants responded differently to the nitrogen source, highlighting the role of cell wall metabolism in inhibiting the growth of NH4+-stressed plants |
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Beschreibung: | Date Completed 09.06.2024 Date Revised 09.06.2024 published: Print-Electronic Citation Status MEDLINE |
ISSN: | 1618-1328 |
DOI: | 10.1016/j.jplph.2024.154264 |