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• W2113707664 abstract "Abstract To gain an understanding of the role of electrical signaling in trees, poplar (Populus trichocarpa, Populus tremula × P. tremuloides) shoots were stimulated by chilling as well as flaming. Two kinds of signal propagation were detected by microelectrode measurements (aphid technique) in the phloem of leaf veins: (1) basipetal, short-distance signaling that led to rapid membrane hyperpolarization caused by K+-efflux within the leaf lamina; and (2) acropetal, long-distance signaling that triggered depolarization of the membrane potential in the leaf phloem. In the latter, the depolarizing signals travel across the stem from the manipulated leaves to adjacent leaves where the net CO2 uptake rate is temporarily depressed toward compensation. With regard to photosystem II, both heat-induced long-distance and short-distance signaling were investigated using two-dimensional “imaging” analysis of chlorophyll fluorescence. Both types of signaling significantly reduced the quantum yield of electron transport through photosystem II. Imaging analysis revealed that the signal that causes yield reduction spreads through the leaf lamina. Coldblocking of the stem proved that the electrical signal transmission via the phloem becomes disrupted, causing the leaf gas exchange to remain unaffected. Calcium-deficient trees showed a marked contrast inasmuch as the amplitude of the electrical signal was distinctly reduced, concomitant with the absence of a significant response in leaf gas exchange upon flame wounding. In summary, the above results led us to conclude that calcium as well as potassium is involved in the propagation of phloem-transmitted electrical signals that evoke specific responses in the photosynthesis of leaves." @default.
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• W2113707664 date "2005-07-22" @default.
• W2113707664 modified "2023-10-10" @default.
• W2113707664 title "Characteristics of Electrical Signals in Poplar and Responses in Photosynthesis" @default.
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• W2113707664 doi "https://doi.org/10.1104/pp.105.064196" @default.
• W2113707664 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1183407" @default.
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