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.

Cytosolic alkalisation and nitric oxide production in UVB-induced stomatal closure in Arabidopsis thaliana

2014 ◽  
Vol 41 (8) ◽  
pp. 803 ◽  
Author(s):  
Xiao-Min Ge ◽  
Yan Zhu ◽  
Jun-Min He
Keyword(s):  
Nitric Oxide ◽  
Arabidopsis Thaliana ◽  
Laser Scanning ◽  
Stomatal Closure ◽  
Guard Cells ◽  
No Production ◽  
Uvb Radiation ◽  
Wild Type ◽  
Cytosolic Ph ◽  
No Scavengers

The role and the interrelationship of cytosolic alkalisation and nitric oxide (NO) in UVB-induced stomatal closure were investigated in Arabidopsis thaliana (L.) Heynh. by stomatal bioassay and laser-scanning confocal microscopy. In response to 0.5 W m–2 UVB radiation, the rise of NO levels in guard cells occurred after cytosolic alkalisation but preceded stomatal closure. UVB-induced NO production and stomatal closure were both inhibited by NO scavengers, nitrate reductase (NR) inhibitors and a Nia2–5/Nia1–2 mutation, and also by butyrate. Methylamine induced NO generation and stomatal closure in the wild-type but not in the Nia2–5/Nia1–2 mutant or wild-type plants pretreated with NO scavengers or NR inhibitors while enhancing the cytosolic pH in guard cells under light. NO generation in wild-type guard cells was largely induced after 60 min of UVB radiation. The defect in UVB-induced NO generation in Nia2–5/Nia1–2 guard cells did not affect the changes of guard cell pH before 60 min of UVB radiation, but prevented the UVB-induced cytosolic alkalisation after 60 min of radiation. Meanwhile, exogenous NO caused a marked rise of cytosolic pH in guard cells. Together, our results show that cytosolic alkalisation and NR-dependent NO production coordinately function in UVB signalling in A. thaliana guard cells.

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.

Fusicoccin inhibits dark-induced stomatal closure by reducing nitric oxide in the guard cells of broad bean

2010 ◽  
Vol 58 (2) ◽  
pp. 81 ◽  
Author(s):  
Xiao-Ping She ◽  
Jin Li ◽  
Ai-Xia Huang ◽  
Xi-Zhu Han
Keyword(s):  
Nitric Oxide ◽  
Butyric Acid ◽  
Laser Scanning ◽  
Broad Bean ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Laser Scanning Confocal Microscopy ◽  
No Removal ◽  
Scanning Confocal Microscopy ◽  
Cytosolic Acidification

By using pharmacological approaches and laser scanning confocal microscopy based on 4,5-diaminofluorescein diacetate (DAF-2DA), the relationship between the inhibition of dark-induced stomatal closure caused by fusicoccin (FC) and the changes of nitric oxide (NO) levels in guard cells in broad bean was studied. The results show that, like 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (c-PTIO), a NO scavenger and NG-nitro-L-Arg-methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), FC inhibited stomatal closure induced by darkness, and reduced the levels of NO in guard cells in darkness, indicating that FC inhibits dark-induced stomatal closure through lessening NO levels in guard cells. In addition, similar to c-PTIO, both FC and butyric acid not only suppressed sodium nitroprusside (SNP)-induced stomatal closure and DAF-2DA fluorescence in guard cells, but also reopened the closed stomata induced by dark and removed NO that had been generated by dark. The results show that both FC and butyric acid cause NO removal in guard cells, and also suggest that FC-caused NO removal is probably associated with cytosolic acidification in guard cells. Taken together, our results show that FC perhaps causes cytosolic acidification in guard cells, consequently induces NO removal and reduces NO levels in guard cells, and finally inhibits stomatal closure induced by dark.

Ethylene inhibits darkness-induced stomatal closure by scavenging nitric oxide in guard cells of Vicia faba

2011 ◽  
Vol 38 (10) ◽  
pp. 767 ◽  
Author(s):  
Xi-Gui Song ◽  
Xiao-Ping She ◽  
Juan Wang ◽  
Yi-Chao Sun
Keyword(s):  
Nitric Oxide ◽  
Vicia Faba ◽  
Plant Hormone ◽  
No Reduction ◽  
Enzyme Commission ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Stomatal Opening ◽  
Physiological Data ◽  
Oxide Synthase

The plant hormone ethylene regulates many aspects of plant growth and development. Despite the well-known relationship between ethylene and stress signalling, the involvement of ethylene in regulating stomatal movement is not completely explored. Here, the role and association between nitric oxide (NO) reduction and the inhibition of darkness-induced stomatal closure by ethylene was studied. Physiological data are provided that both ethylene-releasing compound 2-chloroethylene phosphonic acid (ethephon, ETH) and 1-aminocyclopropane-1-carboxylic acid (ACC), the immediate precursor of ethylene, reduced the levels of NO in Vicia faba L. guard cells, and then induced stomatal opening in darkness. In addition, ACC and ETH not only reduced NO levels in guard cells caused by exogenous NO (derived from sodium nitroprusside, SNP) in light, but also abolished NO that had been generated during a dark period and promoted stomatal opening. Interestingly, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (cPTIO) and hemoglobin (Hb), NO scavenger and the potent scavenger of NO/carbon monoxide (CO), respectively, also reduced NO levels by SNP and darkness. However, the above-mentioned effects of ACC and ETH were dissimilar to that of nitric oxide synthase (enzyme commission 1.14.13.39) inhibitor NG-nitro-L-Arg-methyl ester (L-NAME), which could neither reduce NO levels by SNP nor abolish NO that had been generated in the dark. Thus, it is concluded that ethylene reduces the levels of NO in V. faba guard cells via a pattern of NO scavenging, then induces stomatal opening in the dark.

scholarly journals Estrogen Induces Nitric Oxide Production via Activation of Constitutive Nitric Oxide Synthases in Human Neuroblastoma Cells

Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4550-4557 ◽  
Author(s):  
Yun Xia ◽  
Teresa L. Krukoff
Keyword(s):  
Nitric Oxide ◽  
Neuroblastoma Cells ◽  
No Production ◽  
Tetraacetic Acid ◽  
Acetoxymethyl Ester ◽  
No Release ◽  
Nos Inhibitor ◽  
Neuronal Nos ◽  
Nos Isoforms ◽  
Inducible Nos

Abstract Although it is becoming increasingly evident that nitric oxide (NO) mediates some of estrogen’s actions in the brain, the effects of estrogen on NO production through NO synthases (NOS) in neuronal cells have not yet been identified. Here we assessed changes in NO production induced by 17β-estradiol (E2) in cells of neuronal origin using human SK-N-SH neuroblastoma cells, which we show express all three isoforms of NOS. Involvement of NOS isoforms in E2-induced NO production was examined using isoform-specific NOS inhibitors. E2 (10−10–10−6m) induced rapid increases in NO release and changes in endothelial NOS (eNOS) expression, which were blocked by ICI 182,780, an antagonist of estrogen receptors. Increased levels of NO release and NOS activity induced by E2 were blocked by N5-(1-Imino-3-butenyl)-l-ornithine, a neuronal NOS inhibitor, and N5-(1-Iminoethyl)-l-ornithine, an eNOS inhibitor, but not by 1400W, an inducible NOS inhibitor. These results demonstrate that E2-stimulated NO production occurs via estrogen receptor-mediated activation of the constitutive NOSs, neuronal NOS and eNOS. The E2-induced NO increase was abolished when extracellular Ca2+ was removed from the medium or after the addition of nifedipine, an L-type channel blocker, and was partially inhibited using 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester, an intracellular Ca2+ chelator. However, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid acetoxymethyl ester itself also caused an increase in NO release that was blocked by 1400W, suggesting that inducible NOS mediates this response. Together these data reveal that constitutive NOS activities are responsible for E2- induced NO production in neuroblastoma cells and that differential activation of NOS isoforms in these cells occurs in response to different treatments.

Cytoplasmic Alkalization Mediates Exogenous Nitric Oxide-Induced Stomatal Closure in Vicia faba

2010 ◽  
Vol 36 (3) ◽  
pp. 533-538 ◽  
Author(s):  
Shi-Ling ZHAO ◽  
Li-Rong SUN ◽  
Huan ZHANG ◽  
Li-Ya MA ◽  
Bao-Shi LU ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vicia Faba ◽  
Stomatal Closure ◽  
Exogenous Nitric Oxide

scholarly journals Bcl-2 and Bcl-XL Block Thapsigargin-Induced Nitric Oxide Generation, c-Jun NH2-Terminal Kinase Activity, and Apoptosis

1999 ◽  
Vol 19 (8) ◽  
pp. 5659-5674 ◽  
Author(s):  
Rakesh K. Srivastava ◽  
Steven J. Sollott ◽  
Leila Khan ◽  
Richard Hansford ◽  
Edward G. Lakatta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Caspase 3 ◽  
No Synthase ◽  
Dominant Negative ◽  
Jurkat Cells ◽  
No Production ◽  
Acetoxymethyl Ester ◽  
Jnk Pathway ◽  
Induced Apoptosis ◽  
Jnk Activation

ABSTRACT The proteins Bcl-2 and Bcl-XL prevent apoptosis, but their mechanism of action is unclear. We examined the role of Bcl-2 and Bcl-XL in the regulation of cytosolic Ca2+, nitric oxide production (NO), c-Jun NH2-terminal kinase (JNK) activation, and apoptosis in Jurkat T cells. Thapsigargin (TG), an inhibitor of the endoplasmic reticulum-associated Ca2+ATPase, was used to disrupt Ca2+ homeostasis. TG acutely elevated intracellular free Ca2+ and mitochondrial Ca2+ levels and induced NO production and apoptosis in Jurkat cells transfected with vector (JT/Neo). Buffering of this Ca2+ response with 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA-AM) or inhibiting NO synthase activity with N G-nitro-l-arginine methyl ester hydrochloride (l-NAME) blocked TG-induced NO production and apoptosis in JT/Neo cells. By contrast, while TG produced comparable early changes in the Ca2+ level (i.e., within 3 h) in Jurkat cells overexpressing Bcl-2 and Bcl-XL (JT/Bcl-2 or JT/Bcl-XL), NO production, late (36-h) Ca2+ accumulation, and apoptosis were dramatically reduced compared to those in JT/Neo cells. Exposure of JT/Bcl-2 and JT/Bcl-XL cells to the NO donor,S-nitroso-N-acetylpenacillamine (SNAP) resulted in apoptosis comparable to that seen in JT/Neo cells. TG also activated the JNK pathway, which was blocked by l-NAME. Transient expression of a dominant negative mutant SEK1 (Lys→Arg), an upstream kinase of JNK, prevented both TG-induced JNK activation and apoptosis. A dominant negative c-Jun mutant also reduced TG-induced apoptosis. Overexpression of Bcl-2 or Bcl-XL inhibited TG-induced loss in mitochondrial membrane potential, release of cytochromec, and activation of caspase-3 and JNK. Inhibition of caspase-3 activation blocked TG-induced JNK activation, suggesting that JNK activation occurred downstream of caspase-3. Thus, TG-induced Ca2+ release leads to NO generation followed by mitochondrial changes including cytochrome c release and caspase-3 activation. Caspase-3 activation leads to activation of the JNK pathway and apoptosis. In summary, Ca2+-dependent activation of NO production mediates apoptosis after TG exposure in JT/Neo cells. JT/Bcl-2 and JT/Bcl-XL cells are susceptible to NO-mediated apoptosis, but Bcl-2 and Bcl-XL protect the cells against TG-induced apoptosis by negatively regulating Ca2+-sensitive NO synthase activity or expression.

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.

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