scholarly journals Arabidopsis MLO2 is a negative regulator of sensitivity to extracellular reactive oxygen species

2018 ◽  
Vol 41 (4) ◽  
pp. 782-796 ◽  
Author(s):  
Fuqiang Cui ◽  
Hongpo Wu ◽  
Omid Safronov ◽  
Panpan Zhang ◽  
Rajeev Kumar ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Oxygen Species

scholarly journals A novel stress-inducible CmtR-ESX3-Zn2+ regulatory pathway essential for survival of Mycobacterium bovis under oxidative stress

2020 ◽  
Vol 295 (50) ◽  
pp. 17083-17099
Author(s):  
Xiaohui Li ◽  
Liu Chen ◽  
Jingjing Liao ◽  
Jiechen Hui ◽  
Weihui Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Mycobacterium Bovis ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Oxygen Species ◽  
Bacterial Survival ◽  
Regulatory Pathway ◽  
Host Pathogen Interaction ◽  
Redox Sensor

Reactive oxygen species (ROS) are an unavoidable host environmental cue for intracellular pathogens such as Mycobacterium tuberculosis and Mycobacterium bovis; however, the signaling pathway in mycobacteria for sensing and responding to environmental stress remains largely unclear. Here, we characterize a novel CmtR-Zur-ESX3-Zn2+ regulatory pathway in M. bovis that aids mycobacterial survival under oxidative stress. We demonstrate that CmtR functions as a novel redox sensor and that its expression can be significantly induced under H2O2 stress. CmtR can physically interact with the negative regulator Zur and de-represses the expression of the esx-3 operon, which leads to Zn2+ accumulation and promotion of reactive oxygen species detoxication in mycobacterial cells. Zn2+ can also act as an effector molecule of the CmtR regulator, using which the latter can de-repress its own expression for further inducing bacterial antioxidant adaptation. Consistently, CmtR can induce the expression of EsxH, a component of esx-3 operon involved in Zn2+ transportation that has been reported earlier, and inhibit phagosome maturation in macrophages. Lastly, CmtR significantly contributes to bacterial survival in macrophages and in the lungs of infected mice. Our findings reveal the existence of an antioxidant regulatory pathway in mycobacteria and provide novel information on stress-triggered gene regulation and its association with host–pathogen interaction.

scholarly journals MINK1: The missing link between ROS and its inhibition of Th17 cells

2017 ◽  
Vol 214 (5) ◽  
pp. 1205-1206 ◽  
Author(s):  
Gustavo J. Martinez
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Differentiation ◽  
Th17 Cell ◽  
Th17 Cells ◽  
Reactive Oxygen ◽  
Cell Generation ◽  
Negative Regulator ◽  
Oxygen Species ◽  
Missing Link ◽  
Th17 Cell Differentiation

In this issue of JEM, Fu et al. (https://doi.org/10.1084/jem.20161120) identified the kinase Mink1 as a novel negative regulator of Th17 cell generation. Mink1, activated by reactive oxygen species (ROS), prevents TGF-β activation of Smad2, therefore limiting Th17 cell differentiation.

Upregulation of Id-1 via BMP-2 receptors induces reactive oxygen species in podocytes

2006 ◽  
Vol 291 (3) ◽  
pp. F654-F662 ◽  
Author(s):  
Gregor Pache ◽  
Christina Schäfer ◽  
Sebastian Wiesemann ◽  
Erik Springer ◽  
Max Liebau ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Line ◽  
Kidney Development ◽  
Cell Injury ◽  
Reactive Oxygen ◽  
Cancer Cell Line ◽  
Negative Regulator ◽  
Oxygen Species ◽  
Bmp Receptors

Bone morphogenetic proteins (BMPs) are secreted signaling molecules, which play a major role in kidney development and disease. Here, we show the existence of mRNA for BMP-2 and for the BMP receptors BMPR1A, BMPR1B, BMPRII, ACVR1A, ACVR2, and ACVR2B in differentiated mouse podocytes and the protein expression of BMPR1A in human glomerular podocytes. BMP-2 dose dependently increases the free cytosolic Ca2+ concentration in podocytes proving the existence of a functional receptor in these cells. Recent data indicate that in a myoblastic cell line and in a breast cancer cell line, BMP-2 increases the expression of Id-1, a negative regulator of basic helix-loop-helix transcription factors, but the role of BMP-2 stimulated Id-1 expression in the kidney has not been further characterized. Here, we show that BMP-2 increases the expression of Id-1 in differentiated podocytes. To investigate a role of Id-1 for podocyte function, overexpression of Id-1 was induced in differentiated mouse podocytes. Id-1-overexpressing podocytes show an increased NADPH-dependent production of reactive oxygen species (ROS). This effect can be evoked by BMP-2 and can be antagonized by anti-Id-1 antisense oligonucleotides. The data indicate that BMP-2 may, via an increased expression of Id-1 and an increased generation of ROS, contribute to important cellular functions in podocytes. ROS supposedly play a major role in cell adhesion, cell injury, ion transport, fibrogenesis, angiogenesis and are involved in the pathogenesis of membranous nephropathy.

scholarly journals Proteomic Analysis of NRROS Interactome Reveals the Presence of Chaperones and Mediators of the ERAD Pathway

2018 ◽  
Author(s):  
Rajkumar Noubade ◽  
Qui Phung ◽  
Wilson Phung ◽  
Erik Verschueren ◽  
Laura Lau ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Transmembrane Protein ◽  
Protein Biosynthesis ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Spectrometric Analysis ◽  
Functional Domain ◽  
Oxygen Species ◽  
Er Quality Control ◽  
Erad Pathway

AbstractNegative regulator of reactive oxygen species (NRROS, previously called LRRC33) is a leucine-rich repeat (LRR) domain containing, ER-resident transmembrane protein expressed primarily in lymphoid organs, especially in myeloid cells. We have previously demonstrated that NRROS regulates reactive oxygen species production by phagocytic cells by mediating degradation of NOX2 (gp91phox), a component of NOX2 complex responsible for the oxidative burst in these cells. Since LRR is the only functional domain in NRROS, it is likely to interact with other proteins for its biological functions. Here, by performing immunoprecipitation of NRROS and mass spectrometric analysis, we describe the NRROS interactome in macrophages and demonstrate that NRROS interacts with molecular chaperones/co-chaperones and mediators of the endoplasmic reticulum associated degradation (ERAD) pathway such as calnexin, suggesting a broader role for NRROS in protein biosynthesis and the ER quality control machinery.

scholarly journals Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 320 ◽  
Author(s):  
Shuya Kasai ◽  
Sunao Shimizu ◽  
Yota Tatara ◽  
Junsei Mimura ◽  
Ken Itoh
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Physiological Stress ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Endurance Capacity ◽  
Oxygen Species ◽  
Antioxidant Genes ◽  
Beneficial Effects ◽  
Quantity Control

Reactive oxygen species (ROS) are byproducts of aerobic respiration and signaling molecules that control various cellular functions. Nrf2 governs the gene expression of endogenous antioxidant synthesis and ROS-eliminating enzymes in response to various electrophilic compounds that inactivate the negative regulator Keap1. Accumulating evidence has shown that mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, and induce the expression of antioxidant genes and genes involved in mitochondrial quality/quantity control. Mild physiological stress, such as caloric restriction and exercise, elicits beneficial effects through a process known as “mitohormesis”. Exercise induces NOX4 expression in the heart, which activates Nrf2 and increases endurance capacity. Mice transiently depleted of SOD2 or overexpressing skeletal muscle-specific UCP1 exhibit Nrf2-mediated antioxidant gene expression and PGC1α-mediated mitochondrial biogenesis. ATF4 activation may induce a transcriptional program that enhances NADPH synthesis in the mitochondria and might cooperate with the Nrf2 antioxidant system. In response to severe oxidative stress, Nrf2 induces Klf9 expression, which represses mtROS-eliminating enzymes to enhance cell death. Nrf2 is inactivated in certain pathological conditions, such as diabetes, but Keap1 down-regulation or mtROS elimination rescues Nrf2 expression and improves the pathology. These reports aid us in understanding the roles of Nrf2 in pathophysiological alterations involving mtROS.

scholarly journals NTRC and Chloroplast-Generated Reactive Oxygen Species Regulate Pseudomonas syringae pv. tomato Disease Development in Tomato and Arabidopsis

2012 ◽  
Vol 25 (3) ◽  
pp. 294-306 ◽  
Author(s):  
Yasuhiro Ishiga ◽  
Takako Ishiga ◽  
Tamding Wangdi ◽  
Kirankumar S. Mysore ◽  
Srinivasa Rao Uppalapati
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pseudomonas Syringae ◽  
Function Analysis ◽  
Virulent Strain ◽  
Reactive Oxygen ◽  
Forward Genetics ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Oxygen Species

Coronatine (COR)-producing pathovars of Pseudomonas syringae, including pvs. tomato, maculicola, and glycinea, cause important diseases on tomato, crucifers, and soybean, respectively, and produce symptoms with necrotic lesions surrounded by chlorosis. The chlorosis is mainly attributed to COR. However, the significance of COR-induced chlorosis in localized lesion development and the molecular basis of disease-associated cell death is largely unknown. To identify host (chloroplast) genes that play a role in COR-mediated chlorosis, we used a forward genetics approach using Nicotiana benthamiana and virus-induced gene silencing and identified a gene which encodes 2-Cys peroxiredoxin (Prxs) that, when silenced, produced a spreading hypersensitive or necrosis-like phenotype instead of chlorosis after COR application in a COI1-dependent manner. Loss-of-function analysis of Prx and NADPH-dependent thioredoxin reductase C (NTRC), the central players of a chloroplast redox detoxification system, resulted in spreading accelerated P. syringae pv. tomato DC3000 disease-associated cell death with enhanced reactive oxygen species (ROS) accumulation in a COR-dependent manner in tomato and Arabidopsis. Consistent with these results, virulent strain DC3000 suppressed the expression of Prx and NTRC in Arabidopsis and tomato during pathogenesis. However, interestingly, authentic COR suppressed the expression of Prx and NTRC in tomato but not in Arabidopsis, suggesting that COR in conjunction with other effectors may modulate ROS and cell death in different host species. Taken together, these results indicated that NTRC or Prx function as a negative regulator of pathogen-induced cell death in the healthy tissues that surround the lesions, and COR-induced chloroplast-localized ROS play a role in enhancing the disease-associated cell death.

scholarly journals Caveolin-1 is a negative regulator of NADPH oxidase-derived reactive oxygen species

2014 ◽  
Vol 73 ◽  
pp. 201-213 ◽  
Author(s):  
Feng Chen ◽  
Scott Barman ◽  
Yanfang Yu ◽  
Steven Haigh ◽  
Yusi Wang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Oxygen Species ◽  
Caveolin 1

scholarly journals Transcription Factor NAC075 Delays Leaf Senescence by Deterring Reactive Oxygen Species Accumulation in Arabidopsis

2021 ◽  
Vol 12 ◽  
Author(s):  
Chengcheng Kan ◽  
Yi Zhang ◽  
Hou-Ling Wang ◽  
Yingbai Shen ◽  
Xinli Xia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Transcription Factor ◽  
Leaf Senescence ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Loss Of Function ◽  
Mobility Shift

Leaf senescence is a highly complex genetic process that is finely tuned by multiple layers of regulation. Among them, transcriptional regulation plays a critical role in controlling the initiation and progression of leaf senescence. Here, we found that the NAC transcription factor NAC075 functions as a novel negative regulator of leaf senescence. Loss of function of NAC075 promotes leaf senescence in an age-dependent manner, whereas constitutive overexpression of NAC075 delays senescence in Arabidopsis. Transcriptome analysis revealed that transcript levels of antioxidant enzymes such as catalase (CAT), ascorbate peroxidase (APX), and superoxide dismutase (SOD) are significantly suppressed in nac075 mutants compared with wild-type plants. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) analyses revealed that NAC075 directly binds the promoter of catalase 2 (CAT2). Moreover, genetic analysis showed that overexpression of CAT2 suppresses the overproduction of reactive oxygen species (ROS) and the early senescence phenotypes of nac075 mutants, suggesting that CAT2 acts downstream of NAC075 to delay leaf senescence by repressing ROS accumulation. Collectively, our findings provide a new regulatory module involving NAC075-CAT2-ROS in controlling leaf senescence in Arabidopsis.

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