[NO may function in the downstream of Ca2+ in ethylene induced stomatal closure in Vicia faba L].
Guo Hua Liu, Jing Liu, Li Hou, Jing Tang, Xin Liu
Abstract
Guo Hua Liu, Jing Liu, Li Hou, Jing Tang, Xin Liu
Abstract
Through pharmacological combined with laser scanning confocal microscope (LSCM) and spectrophotography to study the role of Ca2+ and NO in signaling during Vicia faba L. stomatal movement response to ethylene (Eth). The results showed that treatment with ethephon (0.004%, 0.04%, 0.4%) resulted in a time- and dose-dependent stomatal closure under light. NO scavenger cPTIO, nitrate reductase inhibitor NaN3, or extracellular Ca2+ chelation EGTA reduced ethylene-induced stomatal closure. Moreover, ethylene was shown to enhance nitric oxide levels and, corresponding, nitrate reductase activity. Inhibition of the nitrate reductase diminished ethylene-induced NO production in both stomatal guard cell and leaf. Finally, ethylene-induced NO levels and nitrate reductase activity decreased when Ca2+ was compromised. On the basis of biochemical and pharmacological experimental results, we can conclude that Ca2+ and NO were involved in the signal transduction pathway of ethylene induced stomatal closure. Nitrate reductase-derived NO may represents a novel downstream component of Ca2+ signaling cascade during ethylene-induced stomatal movement in Vicia faba L.
OpenAlex reports 10 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Through pharmacological combined with laser scanning confocal microscope (LSCM) and spectrophotography to study the role of Ca2+ and NO in signaling during Vicia faba L. stomatal movement response to ethylene (Eth). The results showed that treatment with ethephon (0.004%, 0.04%, 0.4%) resulted in a time- and dose-dependent stomatal closure under light. NO scavenger cPTIO, nitrate reductase inhibitor NaN3, or extracellular Ca2+ chelation EGTA reduced ethylene-induced stomatal closure. Moreover, ethylene was shown to enhance nitric oxide levels and, corresponding, nitrate reductase activity. Inhibition of the nitrate reductase diminished ethylene-induced NO production in both stomatal guard cell and leaf. Finally, ethylene-induced NO levels and nitrate reductase activity decreased when Ca2+ was compromised. On the basis of biochemical and pharmacological experimental results, we can conclude that Ca2+ and NO were involved in the signal transduction pathway of ethylene induced stomatal closure. Nitrate reductase-derived NO may represents a novel downstream component of Ca2+ signaling cascade during ethylene-induced stomatal movement in Vicia faba L.
Key concepts: Nitrate reductase, Guard cell, Vicia faba, Ethylene, Ethephon, Nitric oxide, Chemistry, Biophysics