scholarly journals Towards Understanding Extracellular ROS Sensory and Signaling Systems in Plants

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Saijaliisa Kangasjärvi ◽  
Jaakko Kangasjärvi
Keyword(s):  
Reverse Genetics ◽  
Stomatal Closure ◽  
Air Pollutant ◽  
Cellular Functions ◽  
Alarm Signal ◽  
Signaling Systems ◽  
Signaling Function ◽  
Electron Transport Chains ◽  
Response To Stress ◽  
Ros Formation

Reactive Oxygen Species (ROS) are ubiquitous metabolites in all aerobic organisms. Traditionally ROS have been considered as harmful, accidental byproducts of cellular functions involving electron transport chains or electron transfer. However, it is now recognized that controlled production of ROS has significant signaling functions, for example, in pathogen defense, in the regulation of stomatal closure, or in cell-to-cell signaling. ROS formation in subcellular compartments is critical to act as “alarm” signal in the response to stress, and the concept of ROS as primarily signaling substances has emerged. The involvement of ROS in several developmental and inducible processes implies that there must be coordinated function of signaling network(s) that govern ROS responses and subsequent processes. The air pollutant ozone can be used as a useful tool to elucidate the function of apoplastic ROS: O3 degrades in cell wall into various ROS which are interpreted as ROS with signaling function inducing downstream responses. We have used ozone as a tool in mutant screens and transcript profiling-reverse genetics to identify genes involved in processes related to the signaling function of ROS. We review here our recent findings in the elucidation of apoplastic ROS sensing, signaling, and interaction with various symplastic components.

scholarly journals TFEB Signalling-Related MicroRNAs and Autophagy

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 985
Author(s):  
Davide Corà ◽  
Federico Bussolino ◽  
Gabriella Doronzo
Keyword(s):  
Transcriptional Regulation ◽  
Stress Factors ◽  
Cellular Functions ◽  
Post Translational Modifications ◽  
Cellular Processes ◽  
Factor Deficiency ◽  
Transcription Factor Eb ◽  
Important Regulator ◽  
Response To Stress ◽  
Post Transcriptional Regulation

The oncogenic Transcription Factor EB (TFEB), a member of MITF-TFE family, is known to be the most important regulator of the transcription of genes responsible for the control of lysosomal biogenesis and functions, autophagy, and vesicles flux. TFEB activation occurs in response to stress factors such as nutrient and growth factor deficiency, hypoxia, lysosomal stress, and mitochondrial damage. To reach the final functional status, TFEB is regulated in multimodal ways, including transcriptional rate, post-transcriptional regulation, and post-translational modifications. Post-transcriptional regulation is in part mediated by miRNAs. miRNAs have been linked to many cellular processes involved both in physiology and pathology, such as cell migration, proliferation, differentiation, and apoptosis. miRNAs also play a significant role in autophagy, which exerts a crucial role in cell behaviour during stress or survival responses. In particular, several miRNAs directly recognise TFEB transcript or indirectly regulate its function by targeting accessory molecules or enzymes involved in its post-translational modifications. Moreover, the transcriptional programs triggered by TFEB may be influenced by the miRNA-mediated regulation of TFEB targets. Finally, recent important studies indicate that the transcription of many miRNAs is regulated by TFEB itself. In this review, we describe the interplay between miRNAs with TFEB and focus on how these types of crosstalk affect TFEB activation and cellular functions.

scholarly journals Role of D-GADD45 in JNK-Dependent Apoptosis and Regeneration in Drosophila

Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 378 ◽  
Author(s):  
Carlos Camilleri-Robles ◽  
Florenci Serras ◽  
Montserrat Corominas
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control ◽  
Imaginal Discs ◽  
Cellular Functions ◽  
Correct Function ◽  
Response To Stress ◽  
Wing Imaginal Discs ◽  
Harmful Effects

The GADD45 proteins are induced in response to stress and have been implicated in the regulation of several cellular functions, including DNA repair, cell cycle control, senescence, and apoptosis. In this study, we investigate the role of D-GADD45 during Drosophila development and regeneration of the wing imaginal discs. We find that higher expression of D-GADD45 results in JNK-dependent apoptosis, while its temporary expression does not have harmful effects. Moreover, D-GADD45 is required for proper regeneration of wing imaginal discs. Our findings demonstrate that a tight regulation of D-GADD45 levels is required for its correct function both, in development and during the stress response after cell death.

scholarly journals Identification of the C3a Receptor (C3AR1) as the Target of the VGF-derived Peptide TLQP-21 in Rodent Cells

2013 ◽  
Vol 288 (38) ◽  
pp. 27434-27443 ◽  
Author(s):  
Sebastien Hannedouche ◽  
Valerie Beck ◽  
Juliet Leighton-Davies ◽  
Martin Beibel ◽  
Guglielmo Roma ◽  
...  
Keyword(s):  
G Protein ◽  
Cellular Response ◽  
G Protein Coupled Receptors ◽  
Proteolytic Processing ◽  
Rodent Models ◽  
Cellular Functions ◽  
Genome Wide ◽  
Response To Stress ◽  
G Protein Coupled ◽  
Human Receptor

TLQP-21, a peptide derived from VGF (non-acronymic) by proteolytic processing, has been shown to modulate energy metabolism, differentiation, and cellular response to stress. Although extensively investigated, the receptor for this endogenous peptide has not previously been described. This study describes the use of a series of studies that show G protein-coupled receptor-mediated biological activity of TLQP-21 signaling in CHO-K1 cells. Unbiased genome-wide sequencing of the transcriptome from responsive CHO-K1 cells identified a prioritized list of possible G protein-coupled receptors bringing about this activity. Further experiments using a series of defined receptor antagonists and siRNAs led to the identification of complement C3a receptor-1 (C3AR1) as a target for TLQP-21 in rodents. We have not been able to demonstrate so far that this finding is translatable to the human receptor. Our results are in line with a large number of physiological observations in rodent models of food intake and metabolic control, where TLQP-21 shows activity. In addition, the sensitivity of TLQP-21 signaling to pertussis toxin is consistent with the known signaling pathway of C3AR1. The binding of TLQP-21 to C3AR1 not only has effects on signaling but also modulates cellular functions, as TLQP-21 was shown to have a role in directing migration of mouse RAW264.7 cells.

Surface ozone and land-atmosphere coupling

2020 ◽  
Author(s):  
Tamara Emmerichs ◽  
Huug Ouwersloot ◽  
Astrid Kerkweg ◽  
Silvano Fares ◽  
Ivan Mammarella ◽  
...  
Keyword(s):  
Atmospheric Chemistry ◽  
Dry Deposition ◽  
Tropospheric Ozone ◽  
Amazon Basin ◽  
Surface Ozone ◽  
Stomatal Closure ◽  
Circulation Model ◽  
Vapour Pressure Deficit ◽  
Air Pollutant ◽  
Global Models

<p>Surface ozone is a harmful air pollutant, heavily influenced by chemical production and loss processes. Dry deposition to vegetation is a relevant loss process responsible for 20 % of the total tropospheric ozone loss. Its parametrization in atmospheric chemistry models represents a major source of uncertainty for the global tropospheric ozone budget and might account for the mismatch with observations. The model used in this study, the Modular Earth Submodel System (MESSy2) linked to ECHAM5 as atmospheric circulation model (EMAC) is no exception. Like many global models, EMAC employs a “resistances in series” scheme with the major surface deposition via plant stomata which is hardly sensitive to meteorology depending only on solar radiation. Unlike many global models, however, EMAC uses a simplified high resistance for non-stomatal deposition which makes this pathway negligible.                             </p><p>Hence, a revision of the dry deposition scheme of EMAC is desirable. The scheme has been extended with empirical adjustment factors to predict stomatal responses to temperature and vapour pressure deficit. Furthermore, an explicit formulation of humidity depending non-stomatal deposition at the leaf surface (cuticle) has been implemented based on established schemes. Next, the soil moisture availability function for plants has been critically reviewed and modified in order to avoid a stomatal closure where the model shows a strong soil dry bias, e.g. Amazon basin in dry season.</p><p>The last part of the presentation will show comparisons of dry deposition velocities and fluxes comparing simulations with data obtained from four experimental sites where ozone deposition is measured with micrometeorological techniques. The impacts of the changes on daily and seasonal patterns of ozone dry deposition will be discussed with a highlight on surface ozone, global distribution and budget.</p>

scholarly journals Dual Role of Hydrogen Peroxide in Arabidopsis Guard Cells in Response to Sulfur Dioxide

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Huilan Yi ◽  
Xin Liu ◽  
Min Yi ◽  
Gang Chen
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Sulfur Dioxide ◽  
Nadph Oxidase ◽  
Stomatal Closure ◽  
Critical Role ◽  
Guard Cells ◽  
Oxidase Inhibitor ◽  
Air Pollutant ◽  
Low Levels

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.

scholarly journals Site-specific K63 ubiquitinomics reveals post-initiation regulation of ribosomes under oxidative stress

2018 ◽  
Author(s):  
Songhee Back ◽  
Christine Vogel ◽  
Gustavo M. Silva
Keyword(s):  
Oxidative Stress ◽  
Protein Trafficking ◽  
Cellular Functions ◽  
Polyubiquitin Chains ◽  
Site Specific ◽  
High Resolution Mapping ◽  
Translation Factors ◽  
Resolution Mapping ◽  
Response To Stress ◽  
Modified Proteins

AbstractDuring oxidative stress, K63-linked polyubiquitin chains accumulate in the cell and modify a variety of proteins including ribosomes. Knowledge of the precise sites of K63 ubiquitin is key to understanding its function during the response to stress. To identify the sites of K63 ubiquitin, we developed a new mass-spectrometry based method that quantified >1,100 K63 ubiquitination sites in yeast responding to oxidative stress induced by H2O2. We determined that under stress, K63 ubiquitin modified proteins involved in several cellular functions including ion transport, protein trafficking, and translation. The most abundant ubiquitination sites localized to the head of the 40S subunit of the ribosome, modified assembled polysomes, and affected the binding of translation factors. The results suggested a new pathway of post-initiation control of translation during oxidative stress and illustrated the importance of high-resolution mapping of noncanonical ubiquitination events.

scholarly journals Nuclear iASPP determines cell fate by selectively inhibiting either p53 or NF-κB

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Wenjie Ge ◽  
Yudong Wang ◽  
Shanliang Zheng ◽  
Dong Zhao ◽  
Xingwen Wang ◽  
...  
Keyword(s):  
Cell Fate ◽  
Cellular Response ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Functional Interaction ◽  
Signaling Systems ◽  
Optimal Outcomes ◽  
A Cell ◽  
Response To Stress ◽  
Biological Outcomes

Abstractp53 and NF-κBp65 are essential transcription factors (TFs) in the cellular response to stress. Two signaling systems can often be entwined together and generally produce opposing biological outcomes in a cell context-dependent manner. Inhibitor of apoptosis-stimulating protein of p53 (iASPP) has the potential to inhibit both p53 and NF-κBp65, yet how such activities of iASPP are integrated with cancer remains unknown. Here, we utilized different cell models with diverse p53/NF-κBp65 activities. An iASPP(295–828) mutant, which is exclusively located in the nucleus and has been shown to be essential for its inhibitory effects on p53/NF-κBp65, was used to investigate the functional interaction between iASPP and the two TFs. The results showed that iASPP inhibits apoptosis under conditions when p53 is activated, while it can also elicit a proapoptotic effect when NF-κBp65 alone is activated. Furthermore, we demonstrated that iASPP inhibited the transcriptional activity of p53/NF-κBp65, but with a preference toward p53, thereby producing an antiapoptotic outcome when both TFs were simultaneously activated. This may be due to stronger binding between p53 and iASPP than NF-κBp65 and iASPP. Overall, these findings provide important insights into how the activities of p53 and NF-κBp65 are modulated by iASPP. Despite being a well-known oncogene, iASPP may have a proapoptotic role, which will guide the development of iASPP-targeted therapies to reach optimal outcomes in the future.

scholarly journals Sirtuins in Renal Health and Disease

2018 ◽  
Vol 29 (7) ◽  
pp. 1799-1809 ◽  
Author(s):  
Marina Morigi ◽  
Luca Perico ◽  
Ariela Benigni
Keyword(s):  
Energy Homeostasis ◽  
Kidney Diseases ◽  
Renal Physiology ◽  
Cellular Functions ◽  
Evolutionarily Conserved ◽  
Biologic Effects ◽  
Response To Stress ◽  
Health And Disease ◽  
Atp Generation

Sirtuins belong to an evolutionarily conserved family of NAD+-dependent deacetylases that share multiple cellular functions related to proliferation, DNA repair, mitochondrial energy homeostasis, and antioxidant activity. Mammalians express seven sirtuins (SIRT1–7) that are localized in different subcellular compartments. Changes in sirtuin expression are critical in several diseases, including metabolic syndrome, diabetes, cancer, and aging. In the kidney, the most widely studied sirtuin is SIRT1, which exerts cytoprotective effects by inhibiting cell apoptosis, inflammation, and fibrosis together with SIRT3, a crucial metabolic sensor that regulates ATP generation and mitochondrial adaptive response to stress. Here, we provide an overview of the biologic effects of sirtuins and the molecular targets thereof regulating renal physiology. This review also details progress made in understanding the effect of sirtuins in the pathophysiology of chronic and acute kidney diseases, highlighting the key role of SIRT1, SIRT3, and now SIRT6 as potential therapeutic targets. In this context, the current pharmacologic approaches to enhancing the activity of SIRT1 and SIRT3 will be discussed.

scholarly journals c-Jun enhances intestinal epithelial restitution after wounding by increasing phospholipase C-γ1 transcription

2017 ◽  
Vol 312 (4) ◽  
pp. C367-C375 ◽  
Author(s):  
Peng-Yuan Wang ◽  
Shelley R. Wang ◽  
Lan Xiao ◽  
Jie Chen ◽  
Jian-Ying Wang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Phospholipase C ◽  
Proximal Region ◽  
Intestinal Epithelial ◽  
Cellular Functions ◽  
Epithelial Restitution ◽  
Enhancer Binding Protein ◽  
Epithelial Cell Migration ◽  
Response To Stress ◽  
Cell Migration And Proliferation

c-Jun is an activating protein 1 (AP-1) transcription factor and implicated in many aspects of cellular functions, but its exact role in the regulation of early intestinal epithelial restitution after injury remains largely unknown. Phospholipase C-γ1 (PLCγ1) catalyzes hydrolysis of phosphatidylinositol 4,5 biphosphate into the second messenger diacylglycerol and inositol 1,4,5 triphosphate, coordinates Ca2+ store mobilization, and regulates cell migration and proliferation in response to stress. Here we reported that c-Jun upregulates PLCγ1 expression and enhances PLCγ1-induced Ca2+ signaling, thus promoting intestinal epithelial restitution after wounding. Ectopically expressed c-Jun increased PLCγ1 expression at the transcription level, and this stimulation is mediated by directly interacting with AP-1 and CCAAT-enhancer-binding protein (C/EBP) binding sites that are located at the proximal region of the rat PLCγ1 promoter. Increased levels of PLCγ1 by c-Jun elevated cytosolic free Ca2+ concentration and stimulated intestinal epithelial cell migration over the denuded area after wounding. The c-Jun-mediated PLCγ1/Ca2+ signal also plays an important role in polyamine-induced cell migration after wounding because increased c-Jun rescued Ca2+ influx and cell migration in polyamine-deficient cells. These findings indicate that c-Jun induces PLCγ1 expression transcriptionally and enhances rapid epithelial restitution after injury by activating Ca2+ signal.

scholarly journals RPK1 and BAK1 sequentially form complexes with OST1 to regulate ABA-induced stomatal closure

2019 ◽  
Author(s):  
Yun Shang ◽  
Dami Yang ◽  
Yunmi Ha ◽  
Hyun-young Shin ◽  
Kyoung Hee Nam
Keyword(s):  
Water Status ◽  
Stomatal Closure ◽  
Expression Patterns ◽  
Cell Movement ◽  
Guard Cells ◽  
Aba Signaling ◽  
Signaling Systems ◽  
Underlying Mechanisms

Abstract Regulation of plant water status occurs via abscisic acid (ABA)-induced stomatal closure. Open Stomata 1 (OST1) is a critical ABA signaling component regulating this process in guard cells. We previously reported that BRI1-associated receptor kinase 1 (BAK1) positively regulates ABA-induced stomatal closure by interacting with, and phosphorylating OST1. Here, we show that the Receptor-like Protein Kinase 1 (RPK1), previously known to be induced by ABA, is a positive ABA-signaling component in guard cell movement, and interacts with OST1. ABA-inducible expression patterns were observed in RPK1 and OST1, but not in BAK1. We investigated the underlying mechanisms by which the RPK1/OST1 and BAK1/OST1 complexes interact in stomatal guard cells by monitoring the complex formation continuously using FRET analyses. We found that the BAK1/OST1 complex was formed earlier than the RPK1/OST1 complex in response to ABA. In vitro and semi-in vivo kinase assays revealed that a trans-phosphorylation event occurred in the RPK1/OST1 complex, which differs from that in the BAK1/OST1 complex, wherein only OST1 phosphorylation occurred via BAK1. ABA Insensitive 1 (ABI1) only dephosphorylated OST1 in the BAK1/OST1 complex, but dephosphorylated both RPK1 and OST1 proteins in the RPK1/OST1 complex. Our results suggest that there are multiple coordinated ABA signaling systems to regulate stomatal movement.

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