Modulation of potassium transport to increase abiotic stress tolerance in plants

Abstract Potassium is the major cation responsible for the maintenance of the ionic environment in plant cells. Stable potassium homeostasis is indispensable for virtually all cellular functions, and, concomitantly, viability. Plants must cope with environmental changes such as salt or drought that...

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Published in:Journal of experimental botany Vol. 74; no. 19; pp. 5989 - 6005
Main Authors: Mulet, Jose M, Porcel, Rosa, Yenush, Lynne
Format: Journal Article
Language:English
Published: 13-10-2023
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Summary:Abstract Potassium is the major cation responsible for the maintenance of the ionic environment in plant cells. Stable potassium homeostasis is indispensable for virtually all cellular functions, and, concomitantly, viability. Plants must cope with environmental changes such as salt or drought that can alter ionic homeostasis. Potassium fluxes are required to regulate the essential process of transpiration, so a constraint on potassium transport may also affect the plant’s response to heat, cold, or oxidative stress. Sequencing data and functional analyses have defined the potassium channels and transporters present in the genomes of different species, so we know most of the proteins directly participating in potassium homeostasis. The still unanswered questions are how these proteins are regulated and the nature of potential cross-talk with other signaling pathways controlling growth, development, and stress responses. As we gain knowledge regarding the molecular mechanisms underlying regulation of potassium homeostasis in plants, we can take advantage of this information to increase the efficiency of potassium transport and generate plants with enhanced tolerance to abiotic stress through genetic engineering or new breeding techniques. Here, we review current knowledge of how modifying genes related to potassium homeostasis in plants affect abiotic stress tolerance at the whole plant level.
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content type line 23
ISSN:0022-0957
1460-2431
DOI:10.1093/jxb/erad333