scholarly journals ALA-Induced Flavonols Accumulation in Guard Cells Is Involved in Scavenging H2O2 and Inhibiting Stomatal Closure in Arabidopsis Cotyledons

2016 ◽  
Vol 7 ◽  
Author(s):  
Yuyan An ◽  
Xinxin Feng ◽  
Longbo Liu ◽  
Lijun Xiong ◽  
Liangju Wang
Keyword(s):  
Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 885
Author(s):  
Takafumi Shimizu ◽  
Yuri Kanno ◽  
Hiromi Suzuki ◽  
Shunsuke Watanabe ◽  
Mitsunori Seo

The plant hormone abscisic acid (ABA) is actively synthesized in vascular tissues and transported to guard cells to promote stomatal closure. Although several transmembrane ABA transporters have been identified, how the movement of ABA within plants is regulated is not fully understood. In this study, we determined that Arabidopsis NPF4.6, previously identified as an ABA transporter expressed in vascular tissues, is also present in guard cells and positively regulates stomatal closure in leaves. We also found that mutants defective in NPF5.1 had a higher leaf surface temperature compared to the wild type. Additionally, NPF5.1 mediated cellular ABA uptake when expressed in a heterologous yeast system. Promoter activities of NPF5.1 were detected in several leaf cell types. Taken together, these observations indicate that NPF5.1 negatively regulates stomatal closure by regulating the amount of ABA that can be transported from vascular tissues to guard cells.


Author(s):  
Md Tahjib-Ul-Arif ◽  
Shintaro Munemasa ◽  
Toshiyuki Nakamura ◽  
Yoshimasa Nakamura ◽  
Yoshiyuki Murata

Abstract Cytosolic calcium ([Ca2+]cyt) elevation activates plasma membrane anion channels in guard cells, which is required for stomatal closure. However, involvement of the anion channels in the [Ca2+]cyt elevation remains unclear. We investigated the involvement using Arabidopsis thaliana anion channel mutants, slac1-4 slah3-3 and slac1-4 almt12-1. Extracellular calcium induced stomatal closure in the wild-type plants but not in the anion channel mutant plants whereas extracellular calcium induced [Ca2+]cyt elevation both in the wild-type guard cells and in the mutant guard cells. The peak height and the number of the [Ca2+]cyt spike were lower and larger in the slac1-4 slah3-3 than in the wild-type and the height and the number in the slac1-4 almt12-1 were much lower and much larger than in the wild-type. These results suggest that the anion channels are involved in the regulation of [Ca2+]cyt elevation in guard cells.


2015 ◽  
Vol 25 (7) ◽  
pp. 928-935 ◽  
Author(s):  
Christof Lind ◽  
Ingo Dreyer ◽  
Enrique J. López-Sanjurjo ◽  
Katharina von Meyer ◽  
Kimitsune Ishizaki ◽  
...  

2019 ◽  
Vol 116 (11) ◽  
pp. 5015-5020 ◽  
Author(s):  
Chenchen Zhao ◽  
Yuanyuan Wang ◽  
Kai Xun Chan ◽  
D. Blaine Marchant ◽  
Peter J. Franks ◽  
...  

Chloroplast retrograde signaling networks are vital for chloroplast biogenesis, operation, and signaling, including excess light and drought stress signaling. To date, retrograde signaling has been considered in the context of land plant adaptation, but not regarding the origin and evolution of signaling cascades linking chloroplast function to stomatal regulation. We show that key elements of the chloroplast retrograde signaling process, the nucleotide phosphatase (SAL1) and 3′-phosphoadenosine-5′-phosphate (PAP) metabolism, evolved in streptophyte algae—the algal ancestors of land plants. We discover an early evolution of SAL1-PAP chloroplast retrograde signaling in stomatal regulation based on conserved gene and protein structure, function, and enzyme activity and transit peptides of SAL1s in species including flowering plants, the fern Ceratopteris richardii, and the moss Physcomitrella patens. Moreover, we demonstrate that PAP regulates stomatal closure via secondary messengers and ion transport in guard cells of these diverse lineages. The origin of stomata facilitated gas exchange in the earliest land plants. Our findings suggest that the conquest of land by plants was enabled by rapid response to drought stress through the deployment of an ancestral SAL1-PAP signaling pathway, intersecting with the core abscisic acid signaling in stomatal guard cells.


2011 ◽  
Vol 38 (4) ◽  
pp. 303
Author(s):  
Ai-Xia Huang ◽  
Xiao-Ping She

Changes in osmotic pressure can induce stomatal closure to reduce transpirational water loss from plants. In the present work, we investigated the mechanism underlying the perception and transduction of extracellular changes in osmotic pressure in Vicia faba L. guard cells. Using an epidermal strip bioassay and laser-scanning confocal microscopy, we provide evidence that hyperosmotic stress treatment led to stomatal closure and the rapid promotion of hydrogen peroxide (H2O2) production in V. faba guard cells. The effects were largely reduced by H2O2 scavengers ASA, CAT, NADPH oxidase inhibitor DPI and cell wall peroxidase inhibitor SHAM. These results indicate that hyperosmotic stress induces stomatal closure by promoting H2O2 production. Cytochalasin B (CB), latrunculin B (Lat B) and jasplakinolide (JK) inhibited stomatal closure induced by hyperosmotic stress but didn’t prevent the increase of endogenous H2O2 levels, suggesting that microfilaments reorganisation participates in stomatal closure induced by hyperosmotic stress, and may act downstream of H2O2 signalling processes. In addition, we observed splitting of big vacuoles into many small vacuoles in response to hyperosmotic stress and H2O2 treatment, and CB inhibited these changes of vacuoles; stomatal closure was also inhibited. Taken together these results indicate that the stomatal closure in response to hyperosmotic stress may initiate H2O2 generation, and that reorganisation of microfilaments and the changing of vacuoles occurs downstream of H2O2 signalling processes.


2017 ◽  
Vol 29 (12) ◽  
pp. 3186-3197 ◽  
Author(s):  
Ido Nir ◽  
Hagai Shohat ◽  
Irina Panizel ◽  
Neil Olszewski ◽  
Asaph Aharoni ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huilan Yi ◽  
Xin Liu ◽  
Min Yi ◽  
Gang Chen

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plant physiology. Plant can adapt to SO2 stress by controlling stomatal movement, gene expression, and metabolic changes. Here we show clear evidences that SO2-triggered hydrogen peroxide (H2O2) production mediated stomatal closure and cell death in Arabidopsis leaves. High levels of SO2 caused irreversible stomatal closure and decline in guard cell viability, but low levels of SO2 caused reversible stomatal closure. Exogenous antioxidants ascorbic acid (AsA) and catalase (CAT) or Ca2+ antagonists EGTA and LaCl3 blocked SO2-induced stomatal closure and decline in viability. AsA and CAT also blocked SO2-induced H2O2 and [Ca2+]cyt elevation. However, EGTA and LaCl3 inhibited SO2-induced [Ca2+]cyt increase but did not suppress SO2-induced H2O2 elevation. These results indicate that H2O2 elevation triggered stomatal closure and cell death via [Ca2+]cyt signaling in SO2-stimulated Arabidopsis guard cells. NADPH oxidase inhibitor DPI blocked SO2-induced cell death but not the stomatal closure triggered by low levels of SO2, indicating that NADPH oxidase-dependent H2O2 production plays critical role in SO2 toxicity but is not necessary for SO2-induced stomatal closure. Our results suggest that H2O2 production and accumulation in SO2-stimulated plants trigger plant adaptation and toxicity via reactive oxygen species mediating Ca2+ signaling.


2005 ◽  
Vol 32 (3) ◽  
pp. 237 ◽  
Author(s):  
Jun-Min He ◽  
Hua Xu ◽  
Xiao-Ping She ◽  
Xi-Gui Song ◽  
Wen-Ming Zhao

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.


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