Inhibition of darkness-induced stomatal closure by ethylene involves a removal of hydrogen peroxide from guard cells of Vicia faba

2012 ◽  
Vol 59 (3) ◽  
pp. 372-380 ◽  
Author(s):  
X. G. Song ◽  
X. P. She ◽  
J. Wang
Keyword(s):  
Hydrogen Peroxide ◽  
Vicia Faba ◽  
Stomatal Closure ◽  
Guard Cells

Hydrogen sulfide may function downstream of hydrogen peroxide in salt stress-induced stomatal closure in Vicia faba

2019 ◽  
Vol 46 (2) ◽  
pp. 136 ◽  
Author(s):  
Yinli Ma ◽  
Wei Zhang ◽  
Jiao Niu ◽  
Yu Ren ◽  
Fan Zhang
Keyword(s):  
Hydrogen Peroxide ◽  
Hydrogen Sulfide ◽  
Salt Stress ◽  
Vicia Faba ◽  
Laser Scanning ◽  
Stomatal Closure ◽  
Guard Cells ◽  
H2o2 Production ◽  
Diphenylene Iodonium ◽  
Cysteine Desulfhydrase

The roles of hydrogen sulfide (H2S) and hydrogen peroxide (H2O2) in signalling transduction of stomatal closure induced by salt stress were examined by using pharmacological, spectrophotographic and laser scanning confocal microscopic (LSCM) approaches in Vicia faba L. Salt stress resulted in stomatal closure, and this effect was blocked by H2S modulators hypotaurine (HT), aminooxy acetic acid (AOA), hydroxylamine (NH2OH), potassium pyruvate (C3H3KO3) and ammonia (NH3) and H2O2 modulators ascorbic acid (ASA), catalase (CAT), diphenylene iodonium (DPI). Additionally, salt stress induced H2S generation and increased L-/D-cysteine desulfhydrase (L-/D-CDes, pyridoxalphosphate-dependent enzyme) activity in leaves, and caused H2O2 production in guard cells, and these effects were significantly suppressed by H2S modulators and H2O2 modulators respectively. Moreover, H2O2 modulators suppressed salt stress-induced increase of H2S levels and L-/D-CDes activity in leaves as well as stomatal closure of V. faba. However, H2S modulators had no effects on salt stress-induced H2O2 production in guard cells. Altogether, our data suggested that H2S and H2O2 probably are involved in salt stress-induced stomatal closure, and H2S may function downstream of H2O2 in salt stress-induced stomatal movement in V. faba.

scholarly journals Ozone Altered Stomatal/Guard Cell Function: Whole Plant and Single Cell Analysis

2000 ◽  
Author(s):  
Eva J. Pell ◽  
Sarah M. Assmann ◽  
Amnon Schwartz ◽  
Hava Steinberger
Keyword(s):  
Hydrogen Peroxide ◽  
Gas Exchange ◽  
Vicia Faba ◽  
Guard Cell ◽  
Cell Function ◽  
Stomatal Closure ◽  
Relative Sensitivity ◽  
Guard Cells ◽  
Stomatal Opening ◽  
K Channels

Original objectives (revisions from original proposal are highlighted) 1. Elucidate the direct effects O3 and H2O2 on guard cell function, utilizing assays of stomatal response in isolated epidermal peels and whole cell gas exchange. 2. Determine the mechanistic basis of O3 and H2O2 effects on the plasma membrane through application of the electrophysiological technique of patch clamping to isolated guard cells. 3. Determine the relative sensitivity of Israeli cultivars of economically important crops to O3 and determine whether differential leaf conductance responses to O3 can explain relative sensitivity to the air pollutant: transfer of technological expertise to Israel. Background to the topic For a long time O3 has been known to reduce gas exchange in plants; it has however been unclear if O3 can affect the stomatal complex directly. Ion channels are essential in stomatal regulation, but O3 has never before been shown to affect these directly. Major conclusions, solution, achievements 1. Ozone inhibits light-induced stomatal opening in epidermal peels isolated from Vicia faba, Arabidopsis thaliana and Nicotiana tabacum in V. faba plants this leads to reduced assimilation without a direct effect on the photosynthetic apparatus. Stomatal opening is more sensitive to O3 than stomatal closure. 2. Ozone causes inhibition of inward K+ channels (involved in stomatal opening) while no detectable effect is observed o the outward K+ channels (stomatal closure). 3. Hydrogen peroxide inhibits stomatal opening and induces stomatal closure in epidermal peels isolated from Vicia faba. 4. Hydrogen peroxide enhances stomatal closure by increasing K+ efflux from guard cells via outward rectifying K+ channels. 5. Based on epidermal peel experiments we have indirectly shown that Ca2+ may play a role in the guard cell response to O3. However, direct measurement of the guard cell [Ca2+]cyt did not show a response to O3. 6. Three Israeli cultivars of zucchini, Clarita, Yarden and Bareqet, were shown to be relatively sensitive to O3 (0.12 ml1-1 ). 7. Two environmentally important Israeli pine species are adversely affected by O3, even at 0.050 ml1-1 , a level frequently exceeded under local tropospheric conditions. P. brutia may be better equipped than P. halepensis to tolerate O3 stress. 8. Ozone directly affects pigment biosynthesis in pine seedlings, as well as the metabolism of O5 precursors, thus affecting the allocation of resources among various metabolic pathways. 9. Ozone induces activity of antioxidant enzymes, and of ascorbate content i the mesophyll and epidermis cells of Commelina communis L. Implications, both scientific and agricultural We have improved the understanding of how O3 and H2O2 do affect guard cell and stomatal function. We have shown that economical important Israeli species like zucchini and pine are relatively sensitive to O3.

Hydrogen sulfide may function downstream of hydrogen peroxide in mediating darkness-induced stomatal closure in Vicia faba

2018 ◽  
Vol 45 (5) ◽  
pp. 553 ◽  
Author(s):  
Yinli Ma ◽  
Jiao Niu ◽  
Wei Zhang ◽  
Xiang Wu
Keyword(s):  
Hydrogen Peroxide ◽  
Acetic Acid ◽  
Hydrogen Sulfide ◽  
Vicia Faba ◽  
Stomatal Closure ◽  
Guard Cells ◽  
H2o2 Accumulation ◽  
Vicia Faba L ◽  
Cysteine Desulfhydrase ◽  
The Relationship

The relationship between hydrogen sulfide (H2S) and hydrogen peroxide (H2O2) during darkness-induced stomatal closure in Vicia faba L. was investigated by using pharmacological, spectrophotographic and lasers canning confocal microscopic approaches. Darkness-induced stomatal closure was inhibited by H2S scavenger hypotaurine (HT), H2S synthesis inhibitors aminooxy acetic acid (AOA) and hydroxylamine (NH2OH) and potassium pyruvate (N3H3KO3) and ammonia (NH3), which are the products of L-/D-cysteine desulfhydrase (L-/D-CDes). Moreover, darkness induced H2S generation and increased L-/D-CDes activity in leaves of V. faba. H2O2 scavenger and synthesis inhibitors suppressed darkness-induced increase of H2S levels and L-/D-CDes activity as well as stomatal closure in leaves of V. faba. However, H2S scavenger and synthesis inhibitors had no effect on darkness-induced H2O2 accumulation in guard cells of V. faba. From these data it can be deduced that H2S is involved in darkness-induced stomatal closure and acts downstream of H2O2 in V. faba.

Cytokinin- and auxin-induced stomatal opening involves a decrease in levels of hydrogen peroxide in guard cells of Vicia faba

2006 ◽  
Vol 33 (6) ◽  
pp. 573 ◽  
Author(s):  
Xi-Gui Song ◽  
Xiao-Ping She ◽  
Jun-Min He ◽  
Chen Huang ◽  
Tu-sheng Song
Keyword(s):  
Hydrogen Peroxide ◽  
Vicia Faba ◽  
Laser Scanning ◽  
Guard Cells ◽  
Laser Scanning Confocal Microscopy ◽  
Stomatal Opening ◽  
Scanning Confocal Microscopy ◽  
Diphenylene Iodonium ◽  
The Relationship ◽  
Exogenous H2o2

Previous studies have shown that cytokinins and auxins can induce the opening of stomata. However, the mechanism of stomatal opening caused by cytokinins and auxins remains unclear. The purpose of this paper is to investigate the relationship between hydrogen peroxide (H2O2) levels in guard cells and stomatal opening induced by cytokinins and auxins in Vicia faba. By means of stomatal bioassay and laser-scanning confocal microscopy, we provide evidence that cytokinins and auxins reduced the levels of H2O2 in guard cells and induced stomatal opening in darkness. Additionally, cytokinins not only reduced exogenous H2O2 levels in guard cells caused by exposure to light, but also abolished H2O2 that had been generated during a dark period, and promoted stomatal opening, as did ascorbic acid (ASA, an important reducing substrate for H2O2 removal). However, unlike cytokinins, auxins did not reduce exogenous H2O2, did not abolish H2O2 that had been generated in the dark, and therefore did not promote reopening of stoma induced to close in the dark. The above-mentioned effects of auxins were similar to that of diphenylene iodonium (DPI, an inhibitor of the H2O2-generating enzyme NADPH oxidase). Taken together our results indicate that cytokinins probably reduce the levels of H2O2 in guard cells by scavenging, whereas auxins limit H2O2 levels through restraining H2O2 generation, inducing stomatal opening in darkness.

scholarly journals Dual Role of Hydrogen Peroxide in Arabidopsis Guard Cells in Response to Sulfur Dioxide

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huilan Yi ◽  
Xin Liu ◽  
Min Yi ◽  
Gang Chen
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Sulfur Dioxide ◽  
Nadph Oxidase ◽  
Stomatal Closure ◽  
Critical Role ◽  
Guard Cells ◽  
Oxidase Inhibitor ◽  
Air Pollutant ◽  
Low Levels

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and [Ca2+]cyt elevation. However, EGTA and LaCl3 inhibited SO2-induced [Ca2+]cyt increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via [Ca2+]cyt signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.

The role and the interrelationship of hydrogen peroxide and nitric oxide in the UV-B-induced stomatal closure in broad bean

2005 ◽  
Vol 32 (3) ◽  
pp. 237 ◽  
Author(s):  
Jun-Min He ◽  
Hua Xu ◽  
Xiao-Ping She ◽  
Xi-Gui Song ◽  
Wen-Ming Zhao
Keyword(s):  
Vicia Faba ◽  
Laser Scanning ◽  
Broad Bean ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Laser Scanning Confocal Microscopy ◽  
H2o2 Production ◽  
No Production ◽  
No Donor ◽  
Scanning Confocal Microscopy

Previous studies have showed that UV-B can stimulate closure as well as opening of stomata. However, the mechanism of this complex effect of UV-B is not clear. The purpose of this paper is to investigate the role and the interrelationship of H2O2 and NO in UV-B-induced stomatal closure in broad bean (Vicia faba L.). By epidermal strip bioassay and laser-scanning confocal microscopy, we observed that UV-B-induced stomatal closure could be largely prevented not only by NO scavenger c-PTIO or NO synthase (NOS) inhibitor l-NAME, but also by ascorbic acid (ASC, an important reducing substrate for H2O2 removal) or catalase (CAT, the H2O2 scavenger), and that UV-B-induced NO and H2O2 production in guard cells preceded UV-B-induced stomatal closure. These results indicate that UV-B radiation induces stomatal closure by promoting NO and H2O2 production. In addition, c-PTIO, l-NAME, ASC and CAT treatments could effectively inhibit not only UV-B-induced NO production, but also UV-B-induced H2O2 production. Exogenous H2O2-induced NO production and stomatal closure were partly abolished by c-PTIO and l-NAME. Similarly, exogenous NO donor sodium nitroprusside-induced H2O2 production and stomatal closure were also partly reversed by ASC and CAT. These results show a causal and interdependent relationship between NO and H2O2 during UV-B-regulated stomatal movement. Furthermore, the l-NAME data also indicate that the NO in guard cells of Vicia faba is probably produced by a NOS-like enzyme.

Cytosolic alkalization-mediated H2O2 and NO production are involved in darkness-induced stomatal closure in Vicia faba

2013 ◽  
Vol 93 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Yinli Ma ◽  
Xiaoping She ◽  
Shushen Yang
Keyword(s):  
Nitric Oxide ◽  
Vicia Faba ◽  
Butyric Acid ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Weak Acid ◽  
No Production ◽  
Tetraacetic Acid ◽  
Acetoxymethyl Ester ◽  
Cytosolic Ph

Ma, Y., She, X. and Yang, S. 2013. Cytosolic alkalization-mediated H 2 O 2 and NO production are involved in darkness-induced stomatal closure in Vicia faba. Can. J. Plant Sci. 93: 119–130. Darkness raised cytosolic pH, hydrogen peroxide (H2O2) and nitric oxide (NO) levels in guard cells while inducing Vicia faba stomatal closure. These darkness effects were prevented by weak acid butyric acid, H2O2 modulators ascorbic acid (ASA), catalase (CAT), diphenyleneiodonium (DPI) and NO modulators 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), NG-nitro-L-arg-methyl ester (L-NAME) respectively. The data suggest that cytosolic alkalization, H2O2 and NO all participate in darkness-induced stomatal closure. During darkness treatment, pH rise became noticeable at 10 min and peaked at 25 min, while H2O2 and NO production increased significantly at 20 min and reached their maximums at 40 min. The H2O2 and NO levels were increased by methylamine in light and decreased by butyric acid in darkness. The results show that cytosolic alkalization induces H2O2 and NO production. ASA, CAT and DPI suppressed NO production by methylamine, c-PTIO and L-NAME prevented H2O2 generation by methylamine. Calcium chelator 1,2-bis (2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester (BAPTA-AM) and 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) restricted darkness-induced alkalization, H2O2 and NO production and stomatal closure. We suggest that cytosolic alkalization is necessary for H2O2 and NO production during darkness-induced stomatal closure. H2O2 mediates NO synthesis by alkalization, and vice versa. Calcium may act upstream of cytosolic alkalization, H2O2 and NO production, besides its known action downstream of H2O2 and NO.

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