The influence of surfactants on transpiration of strawberry leaves

1993 ◽  
Vol 71 (4) ◽  
pp. 598-601 ◽  
Author(s):  
Marek Kubik ◽  
Lech Michalczuk

Surfactants introduced into strawberry (Fragaria grandiflora Duch. cv. Redgauntlet) leaves in doses of 5.5 × 10−4 – 5.5 × 10−2 μmol per leaf blade decreased the transpiration rate of treated leaves regardless of the electrical charge brought to the membranes. A 5.5 × 10−2 μmol dose of surfactants applied during constant illumination caused almost the same decrease in transpiration as a dose of 7.5 × 10−4 μmol of abscisic acid. Surfactants also accelerated the decrease in transpiration in plants grown in the dark, and there was a consistent rate of solute efflux from guard cells. Fusicoccin applied to plants under the influence of surfactants or abscisic acid caused a sustained increase in the transpiration rate. Mannitol and sucrose caused a temporary increase in transpiration rate. KCl increased transpiration when applied after abscisic acid but decreased transpiration when applied after surfactants. These observations suggest that surfactants and abscisic acid influence the guard cell membrane in different ways and that the electrical charge introduced on the plasmalemma surface is not essential in the regulation of stomatal aperture. Key words: abscisic acid, strawberry, surfactants, transpiration.

2021 ◽  
Author(s):  
Sohail M. Karimi ◽  
Matthias Freund ◽  
Brittney M. Wager ◽  
Michael Knoblauch ◽  
Jörg Fromm ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 885
Author(s):  
Takafumi Shimizu ◽  
Yuri Kanno ◽  
Hiromi Suzuki ◽  
Shunsuke Watanabe ◽  
Mitsunori Seo

The plant hormone abscisic acid (ABA) is actively synthesized in vascular tissues and transported to guard cells to promote stomatal closure. Although several transmembrane ABA transporters have been identified, how the movement of ABA within plants is regulated is not fully understood. In this study, we determined that Arabidopsis NPF4.6, previously identified as an ABA transporter expressed in vascular tissues, is also present in guard cells and positively regulates stomatal closure in leaves. We also found that mutants defective in NPF5.1 had a higher leaf surface temperature compared to the wild type. Additionally, NPF5.1 mediated cellular ABA uptake when expressed in a heterologous yeast system. Promoter activities of NPF5.1 were detected in several leaf cell types. Taken together, these observations indicate that NPF5.1 negatively regulates stomatal closure by regulating the amount of ABA that can be transported from vascular tissues to guard cells.


2011 ◽  
Vol 168 (16) ◽  
pp. 1919-1926 ◽  
Author(s):  
Rayhanur Jannat ◽  
Misugi Uraji ◽  
Miho Morofuji ◽  
Mohammad Muzahidul Islam ◽  
Rachel E. Bloom ◽  
...  

1982 ◽  
Vol 69 (5) ◽  
pp. 1140-1144 ◽  
Author(s):  
Teruo Ogawa ◽  
David Grantz ◽  
John Boyer ◽  
Govindjee

2010 ◽  
Vol 73 (4) ◽  
pp. 790-805 ◽  
Author(s):  
Mengmeng Zhu ◽  
Brigitte Simons ◽  
Ning Zhu ◽  
David G. Oppenheimer ◽  
Sixue Chen

1990 ◽  
Vol 258 (3) ◽  
pp. F568-F582 ◽  
Author(s):  
G. Frindt ◽  
E. E. Windhager

Experiments were carried out to test whether maneuvers believed to increase intracellular Ca2+ concentration [( Ca2+]cell) inhibit Na transport in cortical collecting tubules (CCTs). Unidirectional Na efflux (JNa1----b) and Na influx (JNab----1) were measured isotopically in isolated perfused renal CCTs of rabbits. The animals were either untreated or pretreated with deoxycorticosterone (DOC) for 1-3 wk. To raise [Ca2+]cell, ionomycin or quinidine were added to, or [Na] reduced in, pertubular fluid. In control DOC-pretreated CCTs JNa1----b tended to saturate as luminal Na concentration was increased, reaching 22.9 +/- 1.2 pmol.cm-1.s-1 at 145 mM. In addition, in these CCTs, in contrast to non-DOC-treated tubules, the apical cell membrane was not found to be rate limiting for Na reabsorption as neither amphotericin B nor vasopressin further enhanced JNa1----b. In non-DOC-treated CCTs 10(-6) M ionomycin inhibited JNa1----b by 44.7%. When DOC-pretreated CCTs were exposed to either 10(-6)M ionomycin or 10(-4)M quinidine, JNa1----b was inhibited by 27 and 26%, respectively, while JNab----1 remained unchanged. This ionomycin-induced inhibition was Ca dependent. Exposure of DOC-pretreated CCTs to 5 mM Na-Ringer solution (Na replaced by choline or N-methyl-D-glucamine) for 30 min reduced JNa1----b by 18-30%. The inhibition of JNa1----b caused by any of the three maneuvers was fully reversed upon addition of amphotericin B to the luminal fluid. The results are consistent with the view that a sustained increase in [Ca2+]cell reduces Na transport by inhibition of the rate of Na+ entry across the apical cell membrane.


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