scholarly journals CatB is Critical for Total Catalase Activity and Reduces Bactericidal Effects of Phenazine-1-Carboxylic Acid on Xanthomonas oryzae pv. oryzae and X. oryzae pv. oryzicola

2017 ◽  
Vol 107 (2) ◽  
pp. 163-172 ◽  
Author(s):  
Xiayan Pan ◽  
Jian Wu ◽  
Shu Xu ◽  
Yabing Duan ◽  
Mingguo Zhou

Rice bacterial leaf blight, caused by Xanthomonas oryzae pv. oryzae, and rice bacterial leaf streak, caused by X. oryzae pv. oryzicola, are major diseases of rice. Phenazine-1-carboxylic acid (PCA) is a natural product that is isolated from Pseudomonas spp. and is used to control many important rice diseases in China. We previously reported that PCA disturbs the redox balance, which results in the accumulation of reactive oxygen species in X. oryzae pv. oryzae. In this study, we found that PCA significantly upregulated the transcript levels of catB and katE, which encode catalases, and that PCA sensitivity was reduced when X. oryzae pvs. oryzae and oryzicola were cultured with exogenous catalase. Furthermore, catB deletion mutants of X. oryzae pvs. oryzae and oryzicola showed dramatically decreased total catalase activity, increased sensitivity to PCA, and reduced virulence in rice. In contrast, deletion mutants of srpA and katG, which also encode catalases, exhibited little change in PCA sensitivity. The results indicate that catB in both X. oryzae pvs. oryzae and oryzicola encodes a catalase that helps protect the bacteria against PCA-induced stress.

2017 ◽  
Vol 84 (4) ◽  
Author(s):  
Xiayan Pan ◽  
Shu Xu ◽  
Jian Wu ◽  
Yabing Duan ◽  
Zhitian Zheng ◽  
...  

ABSTRACTXanthomonas oryzaepv. oryzae, which causes rice bacterial leaf blight, andXanthomonas oryzaepv. oryzicola, which causes rice bacterial leaf streak, are important plant-pathogenic bacteria. A member of the adaptor protein family, ankyrin protein, has been investigated largely in humans but rarely in plant-pathogenic bacteria. In this study, a novel ankyrin-like protein, AnkB, was identified inX. oryzaepv. oryzae andX. oryzaepv. oryzicola. The expression ofankBwas significantly upregulated when these bacteria were treated with phenazine-1-carboxylic acid (PCA).ankBis located 58 bp downstream of the genecatB(which encodes a catalase) in both bacteria, and the gene expression ofcatBand catalase activity were reduced followingankBdeletion inX. oryzaepv. oryzae andX. oryzaepv. oryzicola. Furthermore, we demonstrated that AnkB directly interacts with CatB by glutathioneS-transferase (GST) pulldown assays. Deletion ofankBincreased the sensitivity ofX. oryzaepv. oryzae andX. oryzaepv. oryzicola to H2O2and PCA, decreased bacterial biofilm formation, swimming ability, and exopolysaccharide (EPS) production, and also reduced virulence on rice. Together our results indicate that the ankyrin-like protein AnkB has important and conserved roles in antioxidant systems and pathogenicity inX. oryzaepv. oryzae andX. oryzaepv. oryzicola.IMPORTANCEThis study demonstrates that the ankyrin protein AnkB directly interacts with catalase CatB inXanthomonas oryzaepv. oryzae andXanthomonas oryzaepv. oryzicola. Ankyrin protein AnkB can affect the gene expression ofcatB, catalase activity, and sensitivity to H2O2. InXanthomonasspp., the locations of genesankBandcatBand the amino acid sequence of AnkB are highly conserved. It is suggested that in prokaryotes, AnkB plays a conserved role in the defense against oxidative stress.


Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 150
Author(s):  
Kimberly J. Nelson ◽  
Terri Messier ◽  
Stephanie Milczarek ◽  
Alexis Saaman ◽  
Stacie Beuschel ◽  
...  

A central hallmark of tumorigenesis is metabolic alterations that increase mitochondrial reactive oxygen species (mROS). In response, cancer cells upregulate their antioxidant capacity and redox-responsive signaling pathways. A promising chemotherapeutic approach is to increase ROS to levels incompatible with tumor cell survival. Mitochondrial peroxiredoxin 3 (PRX3) plays a significant role in detoxifying hydrogen peroxide (H2O2). PRX3 is a molecular target of thiostrepton (TS), a natural product and FDA-approved antibiotic. TS inactivates PRX3 by covalently adducting its two catalytic cysteine residues and crosslinking the homodimer. Using cellular models of malignant mesothelioma, we show here that PRX3 expression and mROS levels in cells correlate with sensitivity to TS and that TS reacts selectively with PRX3 relative to other PRX isoforms. Using recombinant PRXs 1–5, we demonstrate that TS preferentially reacts with a reduced thiolate in the PRX3 dimer at mitochondrial pH. We also show that partially oxidized PRX3 fully dissociates to dimers, while partially oxidized PRX1 and PRX2 remain largely decameric. The ability of TS to react with engineered dimers of PRX1 and PRX2 at mitochondrial pH, but inefficiently with wild-type decameric protein at cytoplasmic pH, supports a novel mechanism of action and explains the specificity of TS for PRX3. Thus, the unique structure and propensity of PRX3 to form dimers contribute to its increased sensitivity to TS-mediated inactivation, making PRX3 a promising target for prooxidant cancer therapy.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Delin Chen ◽  
Bo Chu ◽  
Xin Yang ◽  
Zhaoqi Liu ◽  
Ying Jin ◽  
...  

AbstractHere, we identify iPLA2β as a critical regulator for p53-driven ferroptosis upon reactive oxygen species (ROS)-induced stress. The calcium-independent phospholipase iPLA2β is known to cleave acyl tails from the glycerol backbone of lipids and release oxidized fatty acids from phospholipids. We found that iPLA2β-mediated detoxification of peroxidized lipids is sufficient to suppress p53-driven ferroptosis upon ROS-induced stress, even in GPX4-null cells. Moreover, iPLA2β is overexpressed in human cancers; inhibition of endogenous iPLA2β sensitizes tumor cells to p53-driven ferroptosis and promotes p53-dependent tumor suppression in xenograft mouse models. These results demonstrate that iPLA2β acts as a major ferroptosis repressor in a GPX4-independent manner. Notably, unlike GPX4, loss of iPLA2β has no obvious effect on normal development or cell viability in normal tissues but iPLA2β plays an essential role in regulating ferroptosis upon ROS-induced stress. Thus, our study suggests that iPLA2β is a promising therapeutic target for activating ferroptosis-mediated tumor suppression without serious toxicity concerns.


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1647
Author(s):  
Wen-Jing Liu ◽  
Ying-Xue Huang ◽  
Wei Wang ◽  
Ye Zhang ◽  
Bing-Jie Liu ◽  
...  

Development of resistance to therapy in ovarian cancer is a major hinderance for therapeutic efficacy; however, new mechanisms of the resistance remain to be elucidated. NADPH oxidase 4 (NOX4) is responsible for higher NADPH activity to increase reactive oxygen species (ROS) production. In this study, we showed that higher levels of NOX4 were detected in a large portion of human ovarian cancer samples. To understand the molecular mechanism of the NOX4 upregulation, we showed that NOX4 expression was induced by HIF-1α and growth factor such as IGF-1. Furthermore, our results indicated that NOX4 played a pivotal role in chemotherapy and radiotherapy resistance in ovarian cancer cells. We also demonstrated that NOX4 knockdown increased sensitivity of targeted therapy and radiotherapy through decreased expression of HER3 (ERBB3) and NF-κB p65. Taken together, we identified a new HIF-1α/NOX4 signal pathway which induced drug and radiation resistance in ovarian cancer. The finding may provide a new option to overcome the therapeutic resistance of ovarian cancer in the future.


2019 ◽  
Vol 8 (1) ◽  
pp. 90-95
Author(s):  
Alexander Sergeevich Petukhov ◽  
Nikolay Aleksandrovich Khritokhin ◽  
Tatyana Anatolyevna Kremleva ◽  
Galina Aleksandrovna Petukhova

Pollutants entering plants cells are able to cause biochemical malfunction, including lipid peroxidation, which leads to the change in antioxidant system activity. Sustaining redox balance in cells is a required condition of plants survival in conditions of anthropogenic pollution. The goal of this research was the investigation of catalase activity in meadow grass, wild vetch, red clover, coltsfoot and chamomile near various factories of Tyumen. Plants were gathered near the highway as well as close to the metallurgical plant, engine factory, oil refinery and accumulator plants. The change in catalase activity in the cells of plants turned out to be species-specific. The decrease in catalase activity was observed in the meadow grass and wild vetch cells, while in coltsfoot, red clover and chamomile both decrease and increase in enzyme activity was obtained. Pollutants from all the examined factories affected more or less on the catalase activity, but the greatest effect was registered near the metallurgical factory, that probably related to high heavy metal concentration in plants. The lowest effect on catalase activity, compared to control, was observed near the highway.


Plant Disease ◽  
2015 ◽  
Vol 99 (12) ◽  
pp. 1853-1853 ◽  
Author(s):  
T. T. Tran ◽  
N. V. Nga ◽  
P. T. Ngan ◽  
N. T. Hong ◽  
B. Szurek ◽  
...  

2021 ◽  
Vol 22 (23) ◽  
pp. 12953
Author(s):  
Chengqian Wei ◽  
Junjie Huang ◽  
Yu Wang ◽  
Yifang Chen ◽  
Xin Luo ◽  
...  

A series of new oxadiazole sulfone derivatives containing an amide moiety was synthesized based on fragment virtual screening to screen high-efficiency antibacterial agents for rice bacterial diseases. All target compounds showed greater bactericidal activity than commercial bactericides. 3-(4-fluorophenyl)-N-((5-(methylsulfonyl)-1,3,4-oxadiazol-2-yl)methyl)acrylamide (10) showed excellent antibacterial activity against Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola, with EC50 values of 0.36 and 0.53 mg/L, respectively, which were superior to thiodiazole copper (113.38 and 131.54 mg/L) and bismerthiazol (83.07 and 105.90 mg/L). The protective activity of compound 10 against rice bacterial leaf blight and rice bacterial leaf streak was 43.2% and 53.6%, respectively, which was superior to that of JHXJZ (34.1% and 26.4%) and thiodiazole copper (33.0% and 30.2%). The curative activity of compound 10 against rice bacterial leaf blight and rice bacterial leaf streak was 44.5% and 51.7%, respectively, which was superior to that of JHXJZ (32.6% and 24.4%) and thiodiazole copper (27.1% and 28.6%). Moreover, compound 10 might inhibit the growth of Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola by affecting the extracellular polysaccharides, destroying cell membranes, and inhibiting the enzyme activity of dihydrolipoamide S-succinyltransferase.


2018 ◽  
Vol 13 ◽  
pp. 117727191875539 ◽  
Author(s):  
Seema Kumari ◽  
Anil Kumar Badana ◽  
Murali Mohan G ◽  
Shailender G ◽  
RamaRao Malla

Background: Cancer is one of the major heterogeneous disease with high morbidity and mortality with poor prognosis. Elevated levels of reactive oxygen species (ROS), alteration in redox balance, and deregulated redox signaling are common hallmarks of cancer progression and resistance to treatment. Mitochondria contribute mainly in the generation of ROS during oxidative phosphorylation. Elevated levels of ROS have been detected in cancers cells due to high metabolic activity, cellular signaling, peroxisomal activity, mitochondrial dysfunction, activation of oncogene, and increased enzymatic activity of oxidases, cyclooxygenases, lipoxygenases, and thymidine phosphorylases. Cells maintain intracellular homeostasis by developing an immense antioxidant system including catalase, superoxide dismutase, and glutathione peroxidase. Besides these enzymes exist an important antioxidant glutathione and transcription factor Nrf2 which contribute in balancing oxidative stress. Reactive oxygen species–mediated signaling pathways activate pro-oncogenic signaling which eases in cancer progression, angiogenesis, and survival. Concomitantly, to maintain ROS homeostasis and evade cancer cell death, an increased level of antioxidant capacity is associated with cancer cells. Conclusions: This review focuses the role of ROS in cancer survival pathways and importance of targeting the ROS signal involved in cancer development, which is a new strategy in cancer treatment.


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