Pollen PCP-B peptides unlock a stigma peptide–receptor kinase gating mechanism for pollination

Science ◽  
2021 ◽  
Vol 372 (6538) ◽  
pp. 171-175
Author(s):  
Chen Liu ◽  
Lianping Shen ◽  
Yu Xiao ◽  
David Vyshedsky ◽  
Chao Peng ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Oxygen Species ◽  
Receptor Kinase ◽  
Peptide Receptor ◽  
Pollen Hydration ◽  
Gating Mechanism ◽  
Pollen Coat ◽  
Rapid Alkalinization Factor ◽  
Pollen Coat Protein ◽  
Distinct Peptide

Sexual reproduction in angiosperms relies on precise communications between the pollen and pistil. The molecular mechanisms underlying these communications remain elusive. We established that in Arabidopsis, a stigmatic gatekeeper, the ANJEA–FERONIA (ANJ–FER) receptor kinase complex, perceives the RAPID ALKALINIZATION FACTOR peptides RALF23 and RALF33 to induce reactive oxygen species (ROS) production in the stigma papillae, whereas pollination reduces stigmatic ROS, allowing pollen hydration. Upon pollination, the POLLEN COAT PROTEIN B-class peptides (PCP-Bs) compete with RALF23/33 for binding to the ANJ–FER complex, leading to a decline of stigmatic ROS that facilitates pollen hydration. Our results elucidate a molecular gating mechanism in which distinct peptide classes from pollen compete with stigma peptides for interaction with a stigmatic receptor kinase complex, allowing the pollen to hydrate and germinate.

scholarly journals Loss of a plant receptor kinase recruits beneficial rhizosphere-associated Pseudomonas

2020 ◽  
Author(s):  
Yi Song ◽  
Andrew J. Wilson ◽  
Xue-Cheng Zhang ◽  
David Thoms ◽  
Reza Sohrabi ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Molecular Mechanisms ◽  
Natural Soil ◽  
Oxygen Species ◽  
Receptor Kinase ◽  
Biotic And Abiotic Stress ◽  
Beneficial Bacteria ◽  
Gene Encoding ◽  
Rhizosphere Microbiome ◽  
Transplant Experiments

AbstractMaintaining microbiome structure is critical for the health of both plants1 and animals2. In plants, enrichment of beneficial bacteria is associated with advantageous outcomes including protection from biotic and abiotic stress3,4. However, the genetic and molecular mechanisms by which plants enrich for specific beneficial microbes without general dysbiosis have remained elusive. Here we show that through regulation of NADPH oxidase, FERONIA kinase negatively regulates beneficial Pseudomonas fluorescens in the Arabidopsis rhizosphere microbiome. By rescreening a collection of Arabidopsis mutants that affect root immunity under gnotobiotic conditions, followed by microbiome sequencing in natural soil, we identified a FERONIA mutant (fer-8) with a rhizosphere microbiome enriched in P. fluorescens without phylum-level dysbiosis. Using microbiome transplant experiments, we found that the fer-8 microbiome was beneficial and promoted plant growth. The effect of FER on rhizosphere Pseudomonads was independent of its immune coreceptor function, role in development, and jasmonic acid autoimmunity. We found that the fer-8 mutant has reduced basal levels of reactive oxygen species (ROS) in roots and that mutants deficient in NADPH oxidase showed elevated rhizosphere Pseudomonad levels. Overexpression of the ROP2 gene (encoding a client of FER and positive regulator of NADPH oxidase5) in fer-8 plants suppressed Pseudomonad overgrowth. This work shows that FER-mediated ROS production regulates levels of beneficial Pseudomonads in the rhizosphere microbiome.

Trilobatin Protects Cardiomyocytes from Hypoxia/ Reperfusion Injury by Regulating the Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Pathway

2020 ◽  
Vol 19 (2) ◽  
pp. 133-138
Author(s):  
Wenyu Chen ◽  
Hui He
Keyword(s):  
Heme Oxygenase ◽  
Molecular Mechanisms ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Cellular Injury ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Natural Plant ◽  
Induced Changes

Trilobatin is a natural plant-derived glycosylated flavonoid that has been shown to exhibit multiple beneficial pharmacologic activities including protection of heart against H/R-induced cardiomyocyte injury. However, the molecular mechanisms underlying protection from H/R-induced cardiomyocyte injury remain unknown. Using H9C2 cells as a model, we examined the effect of trilobatin on H/R-induced cellular injury, apoptosis, and generation of reactive oxygen species. The results showed that trilobatin protected H9C2 cells not only from cell death and apoptosis, but also counteracted H/R-induced changes in malondialdehyde, superoxide dismutase, glutathione, and glutathione peroxidase. The evaluation of the mechanism underlying the effect of trilobatin on protection from H/R-induced cellular injury suggested changes in the regulation of nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway.

scholarly journals Metformin Protects H9C2 Cardiomyocytes from High-Glucose and Hypoxia/Reoxygenation Injury via Inhibition of Reactive Oxygen Species Generation and Inflammatory Responses: Role of AMPK and JNK

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Mingyan Hu ◽  
Ping Ye ◽  
Hua Liao ◽  
Manhua Chen ◽  
Feiyan Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound C ◽  
Hypoxia Reoxygenation

Metformin is a first-line drug for the management of type 2 diabetes. Recent studies suggested cardioprotective effects of metformin against ischemia/reperfusion injury. However, it remains elusive whether metformin provides direct protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes under normal or hyperglycemic conditions. This study in H9C2 rat cardiomyoblasts was designed to determine cell viability under H/R and high-glucose (HG, 33 mM) conditions and the effects of cotreatment with various concentrations of metformin (0, 1, 5, and 10 mM). We further elucidated molecular mechanisms underlying metformin-induced cytoprotection, especially the possible involvement of AMP-activated protein kinase (AMPK) and Jun NH(2)-terminal kinase (JNK). Results indicated that 5 mM metformin improved cell viability, mitochondrial integrity, and respiratory chain activity under HG and/or H/R (P<0.05). The beneficial effects were associated with reduced levels of reactive oxygen species generation and proinflammatory cytokines (TNF-α, IL-1α, and IL-6) (P<0.05). Metformin enhanced phosphorylation level of AMPK and suppressed HG + H/R induced JNK activation. Inhibitor of AMPK (compound C) or activator of JNK (anisomycin) abolished the cytoprotective effects of metformin. In conclusion, our study demonstrated for the first time that metformin possessed direct cytoprotective effects against HG and H/R injury in cardiac cells via signaling mechanisms involving activation of AMPK and concomitant inhibition of JNK.

scholarly journals Intraperitoneal Triamcinolone Reduces Postoperative Adhesions, Possibly through Alteration of Mitochondrial Function

2022 ◽  
Vol 11 (2) ◽  
pp. 301
Author(s):  
Neeraja Purandare ◽  
Katherine J. Kramer ◽  
Paige Minchella ◽  
Sarah Ottum ◽  
Christopher Walker ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Function ◽  
Molecular Mechanisms ◽  
Human Fibroblasts ◽  
Reactive Oxygen ◽  
Retrospective Chart Review ◽  
Oxygen Species ◽  
Abdominal Myomectomy ◽  
Hypoxic Conditions

Adhesions frequently occur postoperatively, causing morbidity. In this noninterventional observational cohort study, we enrolled patients who presented for repeat abdominal surgery, after a history of previous abdominal myomectomy, from March 1998 to June 20210 at St. Vincent’s Catholic Medical Centers. The primary outcome of this pilot study was to compare adhesion rates, extent, and severity in patients who were treated with intraperitoneal triamcinolone acetonide during the initial abdominal myomectomy (n = 31) with those who did not receive any antiadhesion interventions (n = 21), as documented on retrospective chart review. Adhesions were blindly scored using a standard scoring system. About 32% of patients were found to have adhesions in the triamcinolone group compared to 71% in the untreated group (p < 0.01). Compared to controls, adhesions were significantly less in number (0.71 vs. 2.09, p < 0.005), severity (0.54 vs. 1.38, p < 0.004), and extent (0.45 vs. 1.28, p < 0.003). To understand the molecular mechanisms, human fibroblasts were incubated in hypoxic conditions and treated with triamcinolone or vehicle. In vitro studies showed that triamcinolone directly prevents the surge of reactive oxygen species triggered by 2% hypoxia and prevents the increase in TGF-β1 that leads to the irreversible conversion of fibroblasts to an adhesion phenotype. Triamcinolone prevents the increase in reactive oxygen species through alterations in mitochondrial function that are HIF-1α-independent. Controlling mitochondrial function may thus allow for adhesion-free surgery and reduced postoperative complications.

scholarly journals Inhibition of iNOS protects against the deleterious effects of sub-lethal sepsis and ethanol in the cardiorenal system

2021 ◽  
Author(s):  
Arthur H. Sousa ◽  
Gabriel T. Do Vale ◽  
Jose A Nascimento ◽  
Wanessa Mayumi Carvalho Awata ◽  
Carla Brigagão Pacheco da Silva ◽  
...  
Keyword(s):  
Biochemical Analysis ◽  
Molecular Mechanisms ◽  
Renal Cortex ◽  
Cecal Ligation ◽  
Selective Inhibitor ◽  
Oxygen Species ◽  
Cecal Ligation And Puncture ◽  
Post Surgery ◽  
Lethal Sepsis ◽  
Pro Inflammatory Cytokines

We tested the hypothesis that ethanol would aggravate the deleterious effects of sub-lethal cecal ligation and puncture (SL-CLP) sepsis in the cardiorenal system and that inhibition of iNOS would prevent such response. Male C57BL/6 mice were treated with ethanol for 12 weeks. One hour before SL-CLP surgery, mice were treated with N6-(1-Iminoethyl)-lysine (L-NIL, 5 mg/kg, i.p), a selective inhibitor of iNOS. A second dose of L-NIL was administered 24 h after SL-CLP surgery. Mice were killed 48 h post-surgery and blood, the renal cortex and left ventricle (LV) were collected for biochemical analysis. L-NIL attenuated the increase in serum creatinine levels induced by ethanol, but not by SL-CLP. Ethanol, but not SL-CLP increased creatine kinase (CK)-MB activity and L-NIL did not prevent this response. In the renal cortex, L-NIL prevented the redox imbalance induced by ethanol and SL-CLP. Inhibition of iNOS also decreased lipoperoxidation induced by ethanol and SL-CLP in the LV. L-NIL prevented the increase of pro-inflammatory cytokines and reactive oxygen species (ROS) induced by ethanol and/or SL-CLP in the cardiorenal system, suggesting that iNOS modulated some of the molecular mechanisms that underlie the deleterious effects of both conditions in the cardiorenal system.

scholarly journals Research progress on the antibacterial mechanisms of carvacrol: a mini review

2018 ◽  
Vol 1 (6) ◽  
pp. 71
Author(s):  
Dan Zhang ◽  
Ren-You Gan ◽  
Ying-Ying Ge ◽  
Qiong-Qiong Yang ◽  
Jiao Ge ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Antibacterial Activity ◽  
Quorum Sensing ◽  
Cell Membrane ◽  
Molecular Mechanisms ◽  
Food Preservation ◽  
Research Progress ◽  
Oxygen Species ◽  
Aromatic Plants ◽  
Volatile Oils

Background: Carvacrol is an aromatic phenolic terpenoid widely existing in the volatile oils of thyme, oregano, and some other aromatic plants. Recent studies have found that carvacrol possesses excellent antibacterial activity. In order to provide an updated information about the antibacterial potentials of carvacrol, herein, we summarized recent publications about the antibacterial activity of carvacrol, with special attention paid to its antibacterial molecular mechanisms, including desrupting cell membrane, depleting intracellular ATP, inducing reactive oxygen species, inhibiting efflux pumps, as well as suppressing two important virulence factors, biofilm and quorum sensing. In conclusion, carvacrol is a promising natural antibacterial compound with potential application in food preservation and infection.Keywords：Carvacrol, antibacterial mechanisms, biofilm, quorum sensing

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