Maintenance of mesophyll potassium and regulation of plasma membrane H+-ATPase are associated with physiological responses of tea plants to drought and subsequent rehydration
Drought stress is one of the main factors limiting yield in tea plants. The plant cell's ability to preserve K+ homeostasis is an important strategy for coping with drought stress. Plasma membrane H+-ATPase in the mesophyll cell is important for maintaining membrane potential to regulate K+ tra...
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Published in | The Crop journal Vol. 6; no. 6; pp. 611 - 620 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier B.V
01.12.2018
KeAi Communications Co., Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Drought stress is one of the main factors limiting yield in tea plants. The plant cell's ability to preserve K+ homeostasis is an important strategy for coping with drought stress. Plasma membrane H+-ATPase in the mesophyll cell is important for maintaining membrane potential to regulate K+ transmembrane transport. However, no research to date has investigated the possible relationship between plasma membrane H+-ATPase and mesophyll K+ retention in tea plants under drought and subsequent rehydration conditions. In our experiment, drought stress inhibited plasma membrane H+-ATPase activities and induced net H+ influx, leading to membrane potential depolarization and inducing a massive K+ efflux in tea plant mesophyll cells. Subsequent rehydration increased plasma membrane H+-ATPase activity and induced net H+ efflux, leading to membrane potential hyperpolarization and thus lowering K+ loss. A first downregulated and then upregulated plasma membrane H+-ATPase protein expression level was also observed under drought and subsequent rehydration treatment, a finding in agreement with the change of measured plasma membrane H+-ATPase activities. Taken together, our results suggest that maintenance of mesophyll K+ in tea plants under drought and rehydration is associated with regulation of plasma membrane H+-ATPase activity. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2214-5141 2214-5141 |
DOI: | 10.1016/j.cj.2018.06.001 |