scholarly journals Transcriptomic comparison between Brassica oleracea and rice (Oryza sativa) reveals diverse modulations on cell death in response to Sclerotinia sclerotiorum

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Jiaqin Mei ◽  
Yijuan Ding ◽  
Yuehua Li ◽  
Chaobo Tong ◽  
Hai Du ◽  
...  
Keyword(s):  
Cell Death ◽  
Brassica Oleracea ◽  
Sclerotinia Sclerotiorum ◽  
Transcriptome Sequencing ◽  
Histochemical Staining ◽  
Oxygen Species ◽  
Wrky Transcription Factors ◽  
Ros Accumulation ◽  
Before And After ◽  
Insight Into

Abstract Sclerotinia stem rot caused by Sclerotinia sclerotiorum is a devastating disease of Brassica crops, but not in rice. The leaves of a rice line, a partial resistant (R) and a susceptible (S) Brassica oleracea pool that bulked from a resistance-segregating F2 population were employed for transcriptome sequencing before and after inoculation by S. sclerotiorum for 6 and 12 h. Distinct transcriptome profiles were revealed between B. oleracea and rice in response to S. sclerotiorum. Enrichment analyses of GO and KEGG indicated an enhancement of antioxidant activity in the R B. oleracea and rice, and histochemical staining exhibited obvious lighter reactive oxygen species (ROS) accumulation and cell death in rice and the R B. oleracea as compared to that in the S B. oleracea. Significant enhancement of Ca2+ signalling, a positive regulator of ROS and cell death, were detected in S B. oleracea after inoculation, while it was significantly repressed in the R B. oleracea group. Obvious difference was detected between two B. oleracea groups for WRKY transcription factors, particularly for those regulating cell death. These findings suggest diverse modulations on cell death in host in response to S. sclerotiorum. Our study provides useful insight into the resistant mechanism to S. sclerotiorum.

scholarly journals Insight into the Double-Edged Role of Ferroptosis in Disease

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1790
Author(s):  
Lei Zhang ◽  
Ruohan Jia ◽  
Huizhen Li ◽  
Huarun Yu ◽  
Keke Ren ◽  
...  
Keyword(s):  
Cell Death ◽  
Digestive System ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Disease Treatment ◽  
The Relationship ◽  
Insight Into ◽  
New Strategies ◽  
Research Hotspots

Ferroptosis, a newly described type of iron-dependent programmed cell death that is distinct from apoptosis, necroptosis, and other types of cell death, is involved in lipid peroxidation (LP), reactive oxygen species (ROS) production, and mitochondrial dysfunction. Accumulating evidence has highlighted vital roles for ferroptosis in multiple diseases, including acute kidney injury, cancer, hepatic fibrosis, Parkinson’s disease, and Alzheimer’s disease. Therefore, ferroptosis has become one of the research hotspots for disease treatment and attracted extensive attention in recent years. This review mainly summarizes the relationship between ferroptosis and various diseases classified by the system, including the urinary system, digestive system, respiratory system, nervous system. In addition, the role and molecular mechanism of multiple inhibitors and inducers for ferroptosis are further elucidated. A deeper understanding of the relationship between ferroptosis and multiple diseases may provide new strategies for researching diseases and drug development based on ferroptosis.

scholarly journals Post-stress bacterial cell death mediated by reactive oxygen species

2019 ◽  
Vol 116 (20) ◽  
pp. 10064-10071 ◽  
Author(s):  
Yuzhi Hong ◽  
Jie Zeng ◽  
Xiuhong Wang ◽  
Karl Drlica ◽  
Xilin Zhao
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Bacterial Resistance ◽  
Reactive Oxygen ◽  
Temperature Sensitive ◽  
Oxygen Species ◽  
Stress Genes ◽  
Primary Stress ◽  
Bacterial Cell Death ◽  
Ros Accumulation

Antimicrobial efficacy, which is central to many aspects of medicine, is being rapidly eroded by bacterial resistance. Since new resistance can be induced by antimicrobial action, highly lethal agents that rapidly reduce bacterial burden during infection should help restrict the emergence of resistance. To improve lethal activity, recent work has focused on toxic reactive oxygen species (ROS) as part of the bactericidal activity of diverse antimicrobials. We report that whenEscherichia coliwas subjected to antimicrobial stress and the stressor was subsequently removed, both ROS accumulation and cell death continued to occur. Blocking ROS accumulation by exogenous mitigating agents slowed or inhibited poststressor death. Similar results were obtained with a temperature-sensitive mutational inhibition of DNA replication. Thus, bacteria exposed to lethal stressors may not die during treatment, as has long been thought; instead, death can occur after plating on drug-free agar due to poststress ROS-mediated toxicity. Examples are described in which (i) primary stress-mediated damage was insufficient to kill bacteria due to repair; (ii) ROS overcame repair (i.e., protection from anti-ROS agents was reduced by repair deficiencies); and (iii) killing was reduced by anti-oxidative stress genes acting before stress exposure. Enzymatic suppression of poststress ROS-mediated lethality by exogenous catalase supports a causal rather than a coincidental role for ROS in stress-mediated lethality, thereby countering challenges to ROS involvement in antimicrobial killing. We conclude that for a variety of stressors, lethal action derives, at least in part, from stimulation of a self-amplifying accumulation of ROS that overwhelms the repair of primary damage.

scholarly journals LMM24 Encodes Receptor-Like Cytoplasmic Kinase 109, Which Regulates Cell Death and Defense Responses in Rice

2019 ◽  
Vol 20 (13) ◽  
pp. 3243 ◽  
Author(s):  
Yue Zhang ◽  
Qunen Liu ◽  
Yingxin Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Indica Rice ◽  
Defense Responses ◽  
Rice Cultivar ◽  
Histochemical Staining ◽  
Lesion Mimic ◽  
Ros Accumulation ◽  
Mutant Pool ◽  
Defense Response Genes

Lesion mimic mutants are excellent models for research on molecular mechanisms of cell death and defense responses in rice. We identified a new rice lesion mimic mutant lmm24 from a mutant pool of indica rice cultivar “ZhongHui8015”. The LMM24 gene was identified by MutMap, and LMM24 was confirmed as a receptor-like cytoplasmic kinase 109 by amino acid sequence analysis. The lmm24 mutant displayed dark brown lesions in leaves and growth retardation that were not observed in wild-type ZH8015. The results of histochemical staining and TUNEL assays showed enhanced ROS accumulation and cell death in lmm24. Chloroplast degradation was observed in lmm24 leaves, with decreased expression of photosynthesis-related genes and increased expression of the senescence-induced STAYGREEN (SGR) gene and other senescence-associated genes. Furthermore, lmm24 exhibited enhanced resistance to rice blast fungus Magnaporthe oryzae (M. oryzae) and up-regulation of defense response genes. Our data demonstrate that LMM24 regulates cell death and defense responses in rice.

scholarly journals Dimethyl Sulfoxide Protects Escherichia coli from Rapid Antimicrobial-Mediated Killing

2016 ◽  
Vol 60 (8) ◽  
pp. 5054-5058 ◽  
Author(s):  
Hongfei Mi ◽  
Dai Wang ◽  
Yunxin Xue ◽  
Zhi Zhang ◽  
Jianjun Niu ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Dimethyl Sulfoxide ◽  
Oxygen Species ◽  
Content Type ◽  
Antimicrobial Studies ◽  
Ros Accumulation ◽  
Short Time

ABSTRACTThe contribution of reactive oxygen species (ROS) to antimicrobial lethality was examined by treatingEscherichia coliwith dimethyl sulfoxide (DMSO), an antioxidant solvent frequently used in antimicrobial studies. DMSO inhibited killing by ampicillin, kanamycin, and two quinolones and had little effect on MICs. DMSO-mediated protection correlated with decreased ROS accumulation and provided evidence for ROS-mediated programmed cell death. These data support the contribution of ROS to antimicrobial lethality and suggest caution when using DMSO-dissolved antimicrobials for short-time killing assays.

Delayed germination of Brassica parachinensis seeds by coumarin involves decreased GA4 production and a consequent reduction of ROS accumulation

2021 ◽  
pp. 1-12
Author(s):  
Bing-Xian Chen ◽  
Yuan-Xuan Peng ◽  
Xue-Qin Yang ◽  
Jun Liu
Keyword(s):  
Seed Germination ◽  
Superoxide Anion ◽  
Inhibitory Effect ◽  
Histochemical Staining ◽  
Oxygen Species ◽  
Synthesis Inhibitor ◽  
Ros Accumulation ◽  
Consequent Reduction ◽  
Endogenous Phytohormones ◽  
Germinating Seeds

Abstract The plant allelochemical coumarin effectively inhibits the germination of Brassica parachinensis (B. parachinensis) seeds. Quantification of endogenous phytohormones showed that contents of abscisic acid (ABA), ABA glucose ester, gibberellin A20 (GA20), GA3, GA15, GA24, GA9 and GA4 were higher in germinating seeds than in seedlings. Moreover, the presence of coumarin significantly reduced the content of bioactive GA4 which is thought to positively regulate seed germination. Histochemical staining and spectrophotometry of reactive oxygen species (ROS) revealed that exogenous GA3 and GA4+7 could effectively promote the production of endogenous ROS during germination and that the GA synthesis inhibitor paclobutrazol could effectively inhibit production of ROS. Coumarin significantly inhibited the accumulation of ROS, especially superoxide anion radical ( ${\rm O}_2^{{\cdot}{-}} $ ). This inhibitory effect could be restored by the addition of exogenous GA3 and GA4+7. Coumarin also inhibited the activity of the ROS-degrading enzymes such as superoxide dismutase, catalase and peroxidase as well as β-amylase in seeds and seedlings. Taken together, we propose a model for the regulation of seed germination in B. parachinensis by coumarin, Gas and ROS, in which coumarin may delay seed germination by reducing endogenous GA4, thus decreasing the accumulation of ROS.

scholarly journals Candida albicans infection disturbs the redox homeostasis system and induces reactive oxygen species accumulation for epithelial cell death

2019 ◽  
Vol 20 (4) ◽  
Author(s):  
Tongtong Ren ◽  
Hangqi Zhu ◽  
Lei Tian ◽  
Qilin Yu ◽  
Mingchun Li
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Candida Albicans ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Tissue Damage ◽  
Redox Homeostasis ◽  
Oxygen Species ◽  
Ros Accumulation ◽  
Epithelial Cell Death

ABSTRACT Candida albicans is a common pathogenic fungus with high mortality in immunocompromised patients. However, the mechanism by which C. albicans invades host epithelial cells and causes serious tissue damage remains to be further investigated. In this study, we established the C. albicans–293T renal epithelial cell interaction model to investigate the mechanism of epithelial infection by this pathogen. It was found that C. albicans infection causes severe cell death and reactive oxygen species (ROS) accumulation in epithelial cells. Further investigations revealed that C. albicans infection might up-regulate expression of nicotinamide adenine dinucleotide phosphate (NAPDH) oxidase (NOX), inhibit the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), and suppress the p38–Nrf2–heme oxygenase-1 (HO-1) pathway which plays an important role in the elimination of intracellular ROS. Furthermore, epithelial cell death caused by the fungal infection could be strikingly alleviated by addition of the antioxidant agent glutathione, indicating the critical role of ROS accumulation in cell death caused by the fungus. This study revealed that disturbance of the redox homeostasis system and ROS accumulation in epithelial cells is involved in cell death caused by C. albicans infection, which sheds light on the application of antioxidants in the suppression of tissue damage caused by fungal infection.

Explorations of time and electrochemical potential: opportunities for fresh perspectives on signalling proteins

2014 ◽  
Vol 42 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Julea N. Butt
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytochrome C ◽  
Present Article ◽  
Mitochondrial Respiratory Chain ◽  
Oxygen Species ◽  
Protein Film ◽  
A Cell ◽  
Insight Into ◽  
Ros Reactive Oxygen Species

Apoptosis is triggered by an accumulation of ROS (reactive oxygen species) produced by proteins of the mitochondrial respiratory chain. The levels of ROS are controlled by the activities of mitochondrial redox proteins such as glutaredoxin 2 that help to modulate the susceptibility of a cell to apoptosis. However, once downstream events have resulted in the release of cytochrome c to the cytosol, it is widely considered that cell death is inevitable. Cytochrome c may promote its own release from mitochondria through interactions with the mitochondrial phospholipid cardiolipin (diphosphatidylglycerol). In the present article, spectroelectrochemistry of the cardiolipin complex of cytochrome c and protein film electrochemistry of glutaredoxin 2 are reviewed to illustrate how electrochemical methods provide insight into the properties of signalling proteins.

scholarly journals Morphological, biochemical and molecular hallmarks of programmed cell death in stigmatic papillae of Brassica oleracea L.

Caryologia ◽  
2021 ◽  
Vol 74 (1) ◽  
pp. 117-126
Author(s):  
Aslihan Çetinbaş-Genç ◽  
Cansu Bayam ◽  
Filiz Vardar
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Brassica Oleracea ◽  
Flower Development ◽  
Tunel Staining ◽  
Oxygen Species ◽  
Peroxide Content ◽  
Dense Cytoplasm ◽  
Stigmatic Papillae ◽  
Brassica Oleracea L

The aim of this study is to determine the programmed cell death hallmarks in the stigmatic papillae of Brassica oleracea L. The flower development was divided in two main stages; pre-anthesis and post-anthesis. Programmed cell death hallmarks were examined in parallel to these stages. At pre-anthesis, the stigmatic papillae were ovoid and their dense cytoplasm were rich in insoluble polysaccharide and protein. At post-anthesis, vacuolization and enlargement were quite evident in papillae. Besides, the protein content decreased, but reactive oxygen species increased in comparison to the pre-anthesis stage. Although no significant change in superoxide dismutase activity was detected, catalase activity decreased and hydrogen peroxide content increased at post-anthesis. DAPI stained nuclei appeared rounded and smooth appearance at pre-anthesis, however, some invaginations and fragmentation in nuclei were observed at post-anthesis. Although, TUNEL staining was negative at pre-anthesis, while TUNEL positive reaction was significant in the nuclei of papillae at post-anthesis. In comparison to the pre-anthesis, the number of fragmented nuclei monitored by DAPI and TUNEL staining increased at post-anthesis. 

scholarly journals Lysyl oxidase promotes neuronal ferroptosis exacerbating seizure-induced hippocampal damage

2019 ◽  
Author(s):  
Xiao-Yuan Mao ◽  
Ming-Zhu Jin ◽  
Qin Li ◽  
Ji-Ning Jia ◽  
Qian-Yi Sun ◽  
...  
Keyword(s):  
Cell Death ◽  
Lysyl Oxidase ◽  
Neuronal Loss ◽  
Hippocampal Damage ◽  
Oxygen Species ◽  
Murine Models ◽  
Ht22 Cells ◽  
Related Disease ◽  
Ros Accumulation ◽  
Dependent Cell

AbstractEpilepsy is a serious neurological disorder and characterized by recurrent and unprovoked seizures. A critical pathological factor in the seizure genesis is neuronal loss. However, mechanisms which lead to neuronal death remain elusive. Our present investigation depicted that ferroptosis, a recently discovered iron- and lipid peroxidation-dependent cell death, probably served as a mechanism in murine models of kainic acid (KA)-induced seizures. And treatment with ferroptosis inhibitors ferrostatin-1 (Fer-1), liproxstatin-1 (Lipo-1) or deferoxamine (DFO) significantly suppressed seizure severity and frequency. Using gene expression profiling in HT22 cells after glutamate exposure (a validated ferroptotic cell death model), we identified lysyl oxidase (Lox) as a novel inducer of ferroptosis. Mechanistically, Lox promoted ferroptosis via activation of extracellular regulated protein kinase (ERK)-dependent 5-lipoxygenase (Alox5) phosphorylation at serine 663 residue signaling, subsequent leading to lipid reactive oxygen species (ROS) accumulation. In a murine model of KA-induced seizure, we illustrated that administration of β-aminopropionitrile (BAPN), a specific Lox inhibitor, remarkably prevented seizure generation. Overall, these findings highlight Lox, a novel identified ferroptotic regulator in neurons, serves as a potential target for seizure-related disease including epilepsy.

Sign in / Sign up

Export Citation Format

Share Document