scholarly journals Nitric oxide in guard cells as an important secondary messenger during stomatal closure

2013 ◽  
Vol 4 ◽  
Author(s):  
Gunja Gayatri ◽  
Srinivas Agurla ◽  
Agepati S. Raghavendra
Keyword(s):  
Nitric Oxide ◽  
Stomatal Closure ◽  
Guard Cells ◽  
Secondary Messenger

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.

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.

Lipoxygenase 2 functions in exogenous nitric oxide-induced stomatal closure in Arabidopsis thaliana

2015 ◽  
Vol 42 (11) ◽  
pp. 1019 ◽  
Author(s):  
Yanfeng Sun ◽  
Dong Lv ◽  
Wei Wang ◽  
Wei Xu ◽  
Li Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Arabidopsis Thaliana ◽  
Potassium Channels ◽  
Stomatal Closure ◽  
Normal Growth ◽  
Guard Cells ◽  
Growth Conditions ◽  
Mesophyll Cells ◽  
No Donor ◽  
Leaf Water Loss

Nitric oxide (NO) and lipoxygenase (LOX)-derived oxylipins play important roles in stomatal closure in plants, and LOX–NO crosstalk has been indicated in mesophyll cells. However, whether the crosstalk also exists in guard cells is not clear and the detailed mechanisms remain unknown. Here, we report that exogenous sodium nitroprusside (SNP, a NO donor)-induced stomatal closure was clearly impaired in the AtLOX2 null mutant lox2–1 compared with wild-type (WT) Arabidopsis thaliana (L.) Heynh. Patch clamp analysis showed that the SNP-suppressed activity of inward-rectifying potassium channels in lox2–1 guard cell protoplasts was reduced. Moreover, SNP promoted an increase in cytosolic Ca2+ concentration in guard cells of lox2–1 mutants was inhibited compared with the WT. These results suggest that AtLOX2 plays an important role in NO-induced stomatal closure by affecting the cytosolic Ca2+ concentration increase and the activity of inward-rectifying potassium channels in guard cells. Furthermore, lox2–1 mutants showed a higher rate of leaf water loss and a relatively wider stomatal aperture than the WT under normal growth conditions. These data imply that AtLOX2 might modulate stomatal movement by increasing oxylipin generation in A. thaliana.

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