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.

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.

scholarly journals Hydrogen sulfide induced by hydrogen peroxide mediates darkness-induced stomatal closure in Arabidopsis thaliana

2019 ◽  
Author(s):  
Yinli Ma ◽  
Luhan Shao ◽  
Jiao Niu
Keyword(s):  
Hydrogen Peroxide ◽  
Arabidopsis Thaliana ◽  
Hydrogen Sulfide ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stomatal Movement ◽  
Wild Type ◽  
Salicylhydroxamic Acid ◽  
Diphenylene Iodonium ◽  
Cysteine Desulfhydrase

Abstract Background Whether stomatal movement by darkness in Arabidopsis thaliana is mediated by hydrogen sulfide (H2S) is undiscovered yet, so the interaction between hydrogen peroxide (H2O2) and H2S in the process needs to be elucidated. Results Our results indicated that H2S modulators aminooxy acetic acid (AOA), potassium pyruvate (N3H3KO3) + ammonia (NH3), hydroxylamine (NH2OH), and hypotaurine (HT) inhibited darkness-induced stomatal closure, H2S generation and L-/D-cysteine desulfhydrase (L-/D-CDes) activity increased in wild-type A. thaliana leaves. Darkness induced stomatal closure in wild-type plants, but failed in Atl-cdes and Atd-cdes mutants. Additionally, both L-/D-CDes activity and H2S content were significantly decreased after applying H2O2 modulators salicylhydroxamic acid (SHAM), ascorbic acid (ASA), diphenylene iodonium (DPI), and catalase (CAT) in darkness, but there was almost no effects on H2O2 levels in the presence of AOA, C3H3KO3+NH3, NH2OH, and HT of wild-type plants in darkness. Moreover, darkness couldn't increase H2S content and L-/D-CDes activity of AtrbohF and AtrbohD/F mutants leaves, but increased H2O2 levels in Atl-cdes and Atd-cdes guard cells. Conclusions We observed that L-/D-CDes-generated H2S mediates stomatal closure by darkness, and functions downstream of H2O2 in A. thaliana.

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.

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.

Hydrogen sulfide induced by hydrogen peroxide mediates brassinosteroid-induced stomatal closure of Arabidopsis thaliana

2021 ◽  
Vol 48 (2) ◽  
pp. 195 ◽  
Author(s):  
Yinli Ma ◽  
Luhan Shao ◽  
Wei Zhang ◽  
Fengxi Zheng
Keyword(s):  
Hydrogen Peroxide ◽  
Arabidopsis Thaliana ◽  
Hydrogen Sulfide ◽  
Stomatal Closure ◽  
Guard Cells ◽  
H2o2 Production ◽  
Wild Type ◽  
Synthesis Inhibitor ◽  
In The Wild ◽  
H2s Production

The role of hydrogen sulfide (H2S) and its relationship with hydrogen peroxide (H2O2) in brassinosteroid-induced stomatal closure in Arabidopsis thaliana (L.) Heynh. were investigated. In the present study, 2,4-epibrassinolide (EBR, a bioactive BR) induced stomatal closure in the wild type, the effects were inhibited by H2S scavenger and synthesis inhibitors, and H2O2 scavengers and synthesis inhibitor. However, EBR failed to close the stomata of mutants Atl-cdes, Atd-cdes, AtrbohF and AtrbohD/F. Additionally, EBR induced increase of L-/D-cysteine desulfhydrase (L-/D-CDes) activity, H2S production, and H2O2 production in the wild type, and the effects were inhibited by H2S scavenger and synthesis inhibitors, and H2O2 scavengers and synthesis inhibitor respectively. Furthermore, EBR increased H2O2 levels in the guard cells of AtrbohD mutant, but couldn’t raise H2O2 levels in the guard cells of AtrbohF and AtrbohD/F mutants. Next, scavengers and synthesis inhibitor of H2O2 could significantly inhibit EBR-induced rise of L-/D-CDes activity and H2S production in the wild type, but H2S scavenger and synthesis inhibitors failed to repress EBR-induced H2O2 production. EBR could increase H2O2 levels in the guard cells of Atl-cdes and Atd-cdes mutants, but EBR failed to induce increase of L-/D-CDes activity and H2S production in AtrbohF and AtrbohD/F mutants. Therefore, we conclude that H2S and H2O2 are involved in the signal transduction pathway of EBR-induced stomatal closure. Altogether, our data suggested that EBR induces AtrbohF-dependent H2O2 production and subsequent AtL-CDes-/AtD-CDes-catalysed H2S production, and finally closes stomata in A. thaliana.

scholarly journals Hydrogen sulfide induced by hydrogen peroxide mediates darkness-induced stomatal closure in Arabidopsis thaliana

2019 ◽  
Author(s):  
Yinli Ma ◽  
Luhan Shao ◽  
Jiao Niu
Keyword(s):  
Hydrogen Peroxide ◽  
Arabidopsis Thaliana ◽  
Ascorbic Acid ◽  
Hydrogen Sulfide ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Wild Type ◽  
Activity Increase ◽  
Salicylhydroxamic Acid ◽  
Diphenylene Iodonium

Abstract Background Whether hydrogen sulfide (H2S) mediates darkness-induced stomatal closure in A. thaliana is unknown, and the interaction between H2S and hydrogen peroxide (H2O2) in the process needs to be elucidated. Results Our results indicated that H2S modulators hypotaurine (HT), aminooxy acetic acid (AOA), hydroxylamine (NH2OH) and potassium pyruvate (N3H3KO3)+ammonia (NH3) all inhibited darkness-induced stomatal closure, H2S generation and L-/D-cysteine desulfhydras (L-/D-CDes) activity increase in wild-type A. thaliana leaves. Darkness induced stomatal closure in wild-type plants, but failed in Atl-cdes and Atd-cdes mutants. Additionally, H2S content and L-/D-CDes activity were significantly decreased after application with H2O2 modulators ascorbic acid (ASA), catalase (CAT), diphenylene iodonium (DPI), and salicylhydroxamic acid (SHAM) in darkness, but there is almost no effects on H2O2 levels when in presence of HT, AOA, NH2OH, and C3H3KO3+NH3 in darkness in wild-type plants. Moreover, darkness couldn't increase H2S content and L-/D-CDes activity of AtrbohF and AtrbohD/F mutants leaves, but the levels of H2O2 increased in guard cells of Atl-cdes and Atd-cdes mutants. Conclusions The results suggest that L-/D-CDes-generated H2S mediates darkness-induced stomatal closure, and functions downstream of H2O2 in A. thaliana.

Actin microfilaments and vacuoles are downstream targets of H2O2 signalling pathways in hyperosmotic stress-induced stomatal closure

2011 ◽  
Vol 38 (4) ◽  
pp. 303
Author(s):  
Ai-Xia Huang ◽  
Xiao-Ping She
Keyword(s):  
Osmotic Pressure ◽  
Laser Scanning ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Laser Scanning Confocal Microscopy ◽  
Oxidase Inhibitor ◽  
Hyperosmotic Stress ◽  
H2o2 Production ◽  
H2o2 Treatment ◽  
Scanning Confocal Microscopy

Changes in osmotic pressure can induce stomatal closure to reduce transpirational water loss from plants. In the present work, we investigated the mechanism underlying the perception and transduction of extracellular changes in osmotic pressure in Vicia faba L. guard cells. Using an epidermal strip bioassay and laser-scanning confocal microscopy, we provide evidence that hyperosmotic stress treatment led to stomatal closure and the rapid promotion of hydrogen peroxide (H2O2) production in V. faba guard cells. The effects were largely reduced by H2O2 scavengers ASA, CAT, NADPH oxidase inhibitor DPI and cell wall peroxidase inhibitor SHAM. These results indicate that hyperosmotic stress induces stomatal closure by promoting H2O2 production. Cytochalasin B (CB), latrunculin B (Lat B) and jasplakinolide (JK) inhibited stomatal closure induced by hyperosmotic stress but didn’t prevent the increase of endogenous H2O2 levels, suggesting that microfilaments reorganisation participates in stomatal closure induced by hyperosmotic stress, and may act downstream of H2O2 signalling processes. In addition, we observed splitting of big vacuoles into many small vacuoles in response to hyperosmotic stress and H2O2 treatment, and CB inhibited these changes of vacuoles; stomatal closure was also inhibited. Taken together these results indicate that the stomatal closure in response to hyperosmotic stress may initiate H2O2 generation, and that reorganisation of microfilaments and the changing of vacuoles occurs downstream of H2O2 signalling processes.

Hydrogen peroxide is a common signal for darkness- and ABA-induced stomatal closure in Pisum sativum

2004 ◽  
Vol 31 (9) ◽  
pp. 913 ◽  
Author(s):  
Radhika Desikan ◽  
Man-Kim Cheung ◽  
Andrew Clarke ◽  
Sarah Golding ◽  
Moshe Sagi ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Pisum Sativum ◽  
Nadph Oxidase ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Dependent Manner ◽  
Degenerate Oligonucleotide ◽  
Diphenylene Iodonium ◽  
Common Signal ◽  
Respiratory Burst Oxidase

The requirement for hydrogen peroxide (H2O2) generation and action during stomatal closure induced by darkness and abscisic acid (ABA) was investigated in pea (Pisum sativum L.). Stomatal closure induced by darkness or ABA was inhibited by the H2O2-scavenging enzyme catalase or the antioxidant N-acetyl cysteine (NAC), or by diphenylene iodonium (DPI), an inhibitor of the H2O2-generating enzyme NADPH oxidase. Exogenous H2O2 induced stomatal closure in a dose- and time-dependent manner, and H2O2 was also required for ABA-inhibition of stomatal opening in the light. H2O2 accumulation in guard cells was increased by darkness or ABA, as assessed with the fluorescent dye dichlorodihydrofluorescein diacetate (H2-DCFDA) and confocal microscopy. Such increases were inhibited by catalase, NAC or DPI, consistent with the effects of these compounds on stomatal apertures. Employing polymerase chain reaction (PCR) with degenerate oligonucleotide primers, several NADPH oxidase homologues were identified from pea genomic DNA that had substantial identity to the Arabidopsis thaliana (L.) Heynh. rboh (respiratory burst oxidase homologue) genes. Furthermore, an antibody raised against the tomato rboh identified immunoreactive proteins in epidermal, mesophyll and guard cells.

Inhibition of abscisic acid-induced stomatal closure by ethylene is related to the change of hydrogen peroxide levels in guard cells in broad bean

2011 ◽  
Vol 59 (8) ◽  
pp. 781 ◽  
Author(s):  
XiGui Song ◽  
XiaoPing She ◽  
Juan Wang
Keyword(s):  
Hydrogen Peroxide ◽  
Ascorbic Acid ◽  
Abscisic Acid ◽  
Nadph Oxidase ◽  
Broad Bean ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Diphenylene Iodonium ◽  
Scavenging Enzymes ◽  
Exogenous H2o2

We analysed the role and relationship between hydrogen peroxide (H2O2) reduction and the inhibition of abscisic acid (ABA)-induced stomatal closure by ethylene. Like ascorbic acid (ASA), the most important reducing substrate for H2O2 removal, catalase, one of the H2O2 scavenging enzymes and diphenylene iodonium, an inhibitor of the H2O2-generating enzyme NADPH oxidase, both ethylene-releasing compound 2-chloroethylene phosphonic acid (ethephon, ETH) and 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor of ethylene, were found to inhibit stomatal closure by ABA and to reduce H2O2 levels by ABA in guard cells, indicating that ethylene-caused inhibition of ABA-induced stomatal closure involves reduction of H2O2 levels in guard cells. Additionally, similar to ASA and catalase, ACC/ETH not only suppressed H2O2-induced stomatal closure and H2O2 levels in guard cells treated with exogenous H2O2 in light, but also reopened the stomata which had been closed by ABA and reduced H2O2 levels that had been generated by ABA. The abovementioned effects of ACC and ETH were dissimilar to that of diphenylene iodonium, an inhibitor of the H2O2-generating enzyme NADPH oxidase, which not only had incapability to reduce H2O2 levels by exogenous H2O2 but also could not abolish H2O2 that had been generated by ABA. So we suggest that ethylene probably induces H2O2 removal and reduces H2O2 levels in Vicia faba guard cells, and finally inhibits stomatal closure induced by ABA.

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