Nitric oxide involved in signal transduction of Jasmonic acid-induced stomatal closure of Vicia faba L.

2005 ◽  
Vol 50 (6) ◽  
pp. 520 ◽  
Author(s):  
Xin LIU
2005 ◽  
Vol 50 (6) ◽  
pp. 520-525 ◽  
Author(s):  
Xin Liu ◽  
Wuliang Shi ◽  
Shuqiu Zhang ◽  
Chenghou Lou

2012 ◽  
Vol 11 (10) ◽  
pp. 1644-1653 ◽  
Author(s):  
Jing LIU ◽  
Zhi-hui HOU ◽  
Guo-hua LIU ◽  
Li-xia HOU ◽  
Xin LIU

2010 ◽  
Vol 36 (3) ◽  
pp. 533-538 ◽  
Author(s):  
Shi-Ling ZHAO ◽  
Li-Rong SUN ◽  
Huan ZHANG ◽  
Li-Ya MA ◽  
Bao-Shi LU ◽  
...  

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1229 ◽  
Author(s):  
Jie Zhou ◽  
Zi-xin Xu ◽  
Hui Sun ◽  
Lan-ping Guo

Although smoke-isolated karrikins (KAR1) could regulate secondary metabolism in medicinal plants, the signal transduction mechanism has not been reported. This study highlights the influence of KAR1 on tanshinone I (T-I) production in Salvia miltiorrhiza and the involved signal molecules. Results showed KAR1-induced generation of nitric oxide (NO), jasmonic acid (JA) and T-I in S. miltiorrhiza hairy root. KAR1-induced increase of T-I was suppressed by NO-specific scavenger (cPTIO) and NOS inhibitors (PBITU); JA synthesis inhibitor (SHAM) and JA synthesis inhibitor (PrGall), which indicated that NO and JA play essential roles in KAR1-induced T-I. NO inhibitors inhibited KAR1-induced generation of NO and JA, suggesting NO was located upstream of JA signal pathway. NO-induced T-I production was inhibited by SHAM and PrGall, implying JA participated in transmitting signal NO to T-I accumulation. In other words, NO mediated the KAR1-induced T-I production through a JA-dependent signaling pathway. The results helped us understand the signal transduction mechanism involved in KAR1-induced T-I production and provided helpful information for the production of S. miltiorrhiza hairy root.


2010 ◽  
Vol 61 (13) ◽  
pp. 3749-3758 ◽  
Author(s):  
B. Li ◽  
G. Liu ◽  
Y. Deng ◽  
M. Xie ◽  
Z. Feng ◽  
...  

2013 ◽  
Vol 93 (1) ◽  
pp. 119-130 ◽  
Author(s):  
Yinli Ma ◽  
Xiaoping She ◽  
Shushen Yang

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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