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

2005 ◽  
Vol 50 (6) ◽  
pp. 520-525 ◽  
Author(s):  
Xin Liu ◽  
Wuliang Shi ◽  
Shuqiu Zhang ◽  
Chenghou Lou
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Jasmonic Acid ◽  
Stomatal Closure ◽  
Ofvicia Faba

scholarly journals Smoke-Isolated Karrikins Stimulated Tanshinones Biosynthesis in Salvia miltiorrhiza through Endogenous Nitric Oxide and Jasmonic Acid

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1229 ◽  
Author(s):  
Jie Zhou ◽  
Zi-xin Xu ◽  
Hui Sun ◽  
Lan-ping Guo
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Jasmonic Acid ◽  
Hairy Root ◽  
Salvia Miltiorrhiza ◽  
Signal Molecules ◽  
Synthesis Inhibitor ◽  
Transduction Mechanism ◽  
Signal Transduction Mechanism ◽  
Nos Inhibitors

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.

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 Melatonin and Microglia

2021 ◽  
Vol 22 (15) ◽  
pp. 8296
Author(s):  
Rüdiger Hardeland
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Signal Transduction ◽  
Endothelial Cells ◽  
Bacterial Infections ◽  
Melatonin Receptors ◽  
Sterile Inflammation ◽  
High Complexity ◽  
Anti Inflammatory ◽  
Multiple Signaling

Melatonin interacts in multiple ways with microglia, both directly and, via routes of crosstalk with astrocytes and neurons, indirectly. These effects of melatonin are of relevance in terms of antioxidative protection, not only concerning free-radical detoxification, but also in prevention of processes that cause, promote, or propagate oxidative stress and neurodegeneration, such as overexcitation, toxicological insults, viral and bacterial infections, and sterile inflammation of different grades. The immunological interplay in the CNS, with microglia playing a central role, is of high complexity and includes signaling toward endothelial cells and other leukocytes by cytokines, chemokines, nitric oxide, and eikosanoids. Melatonin interferes with these processes in multiple signaling routes and steps. In addition to canonical signal transduction by MT1 and MT2 melatonin receptors, secondary and tertiary signaling is of relevance and has to be considered, e.g., via the upregulation of sirtuins and the modulation of pro- and anti-inflammatory microRNAs. Many details concerning the modulation of macrophage functionality by melatonin are obviously also applicable to microglial cells. Of particular interest is the polarization toward M2 subtypes instead of M1, i.e., in favor of being anti-inflammatory at the expense of proinflammatory activities, which is well-documented in macrophages but also applies to microglia.

Jasmonic acid: biosynthesis, signal transduction, gene expression

Lipid / Fett ◽  
1998 ◽  
Vol 100 (4-5) ◽  
pp. 139-146 ◽  
Author(s):  
Claus Wasternack ◽  
Otto Miersch ◽  
Robert Kramell ◽  
Bettina Hause ◽  
Jane Ward ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Jasmonic Acid ◽  
Acid Biosynthesis ◽  
Jasmonic Acid Biosynthesis

Phospholipase Dδ is involved in nitric oxide-induced stomatal closure

Planta ◽  
2012 ◽  
Vol 236 (6) ◽  
pp. 1899-1907 ◽  
Author(s):  
Ayelen M. Distéfano ◽  
Denise Scuffi ◽  
Carlos García-Mata ◽  
Lorenzo Lamattina ◽  
Ana M. Laxalt
Keyword(s):  
Nitric Oxide ◽  
Stomatal Closure

scholarly journals Dissection of a Hypoxia-induced, Nitric Oxide–mediated Signaling Cascade

2009 ◽  
Vol 20 (18) ◽  
pp. 4083-4090 ◽  
Author(s):  
Pascale F. Dijkers ◽  
Patrick H. O'Farrell
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signaling Cascade ◽  
S2 Cells ◽  
Signal Transduction System ◽  
Signaling Systems ◽  
Calcium Dependent ◽  
Drosophila S2 Cells ◽  
Oxide Synthase ◽  
Multiple Signaling

Befitting oxygen's key role in life's processes, hypoxia engages multiple signaling systems that evoke pervasive adaptations. Using surrogate genetics in a powerful biological model, we dissect a poorly understood hypoxia-sensing and signal transduction system. Hypoxia triggers NO-dependent accumulation of cyclic GMP and translocation of cytoplasmic GFP-Relish (an NFκB/Rel transcription factor) to the nucleus in Drosophila S2 cells. An enzyme capable of eliminating NO interrupted signaling specifically when it was targeted to the mitochondria, arguing for a mitochondrial NO signal. Long pretreatment with an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling. However, addition shortly before hypoxia was without effect, suggesting that signaling is supported by the prior action of NOS and is independent of NOS action during hypoxia. We implicated the glutathione adduct, GSNO, as a signaling mediator by showing that overexpression of the cytoplasmic enzyme catalyzing its destruction, GSNOR, blocks signaling, whereas knockdown of this activity caused reporter translocation in the absence of hypoxia. In downstream steps, cGMP accumulated, and calcium-dependent signaling was subsequently activated via cGMP-dependent channels. These findings reveal the use of unconventional steps in an NO pathway involved in sensing hypoxia and initiating signaling.

scholarly journals Ultraviolet B Radiation Acts through the Nitric Oxide and cGMP Signal Transduction Pathway to Stimulate Melanogenesis in Human Melanocytes

1996 ◽  
Vol 271 (45) ◽  
pp. 28052-28056 ◽  
Author(s):  
Christine Roméro-Graillet ◽  
Edith Aberdam ◽  
Naïma Biagoli ◽  
William Massabni ◽  
Jean-Paul Ortonne ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signal Transduction Pathway ◽  
Ultraviolet B ◽  
Transduction Pathway ◽  
Ultraviolet B Radiation ◽  
Cgmp Signal ◽  
Human Melanocytes

scholarly journals Nitric Oxide Attenuates Signal Transduction

2001 ◽  
Vol 88 (2) ◽  
pp. 229-236 ◽  
Author(s):  
Hong Li ◽  
Sergey Brodsky ◽  
Mary Basco ◽  
Victor Romanov ◽  
Dino A. De Angelis ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction
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