scholarly journals Recent Progress in the Study of Peroxiredoxin in the Harmful Algal Bloom Species Chattonella marina

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 162
Author(s):  
Yohei Shimasaki ◽  
Koki Mukai ◽  
Yuki Takai ◽  
Xuchun Qiu ◽  
Yuji Oshima
Keyword(s):  
Oxidative Stress ◽  
Growth Phase ◽  
Critical Role ◽  
High Irradiance ◽  
Growth Potential ◽  
Exponential Growth Phase ◽  
Wild Type ◽  
Chattonella Marina ◽  
Strong Light ◽  
Expression Strain

Peroxiredoxin (Prx) is a relatively recently discovered antioxidant enzyme family that scavenges peroxides and is known to be present in organisms from biological taxa ranging from bacteria to multicellular eukaryotes, including photosynthetic organisms. Although there have been many studies of the Prx family in higher plants, green algae, and cyanobacteria, few studies have concerned raphidophytes and dinoflagellates, which are among the eukaryotic algae that cause harmful algal blooms (HABs). In our proteomic study using 2-D electrophoresis, we found a highly expressed 2-Cys peroxiredoxin (2-CysPrx) in the raphidophyte Chattonella marina var. antiqua, a species that induces mass mortality of aquacultured fish. The abundance of the C. marina 2-CysPrx enzyme was highest in the exponential growth phase, during which photosynthetic activity was high, and it then decreased by about a factor of two during the late stationary growth phase. This pattern suggested that 2-CysPrx is a key enzyme involved in the maintenance of high photosynthesis activity. In addition, the fact that the depression of photosynthesis by excessively high irradiance was more severe in the 2-CysPrx low-expression strain (wild type) than in the normal-expression strain (wild type) of C. marina suggested that 2-CysPrx played a critical role in protecting the cell from oxidative stress caused by exposure to excessively high irradiance. In the field of HAB research, estimates of growth potential have been desired to predict the population dynamics of HABs for mitigating damage to fisheries. Therefore, omics approaches have recently begun to be applied to elucidate the physiology of the growth of HAB species. In this review, we describe the progress we have made using a molecular physiological approach to identify the roles of 2-CysPrx and other antioxidant enzymes in mitigating environmental stress associated with strong light and high temperatures and resultant oxidative stress. We also describe results of a survey of expressed Prx genes and their growth-phase-dependent behavior in C. marina using RNA-seq analysis. Finally, we speculate about the function of these genes and the ecological significance of 2-CysPrx, such as its involvement in circadian rhythms and the toxicity of C. marina to fish.

scholarly journals Null Mutations of Group A Streptococcus Orphan Kinase RocA: Selection in Mouse Infection and Comparison with CovS Mutations in Alteration of In Vitro and In Vivo Protease SpeB Expression and Virulence

2016 ◽  
Vol 85 (1) ◽  
Author(s):  
Wenchao Feng ◽  
Dylan Minor ◽  
Mengyao Liu ◽  
Jinquan Li ◽  
Suzanne L. Ishaq ◽  
...  
Keyword(s):  
Gene Expression ◽  
Growth Phase ◽  
Virulence Genes ◽  
Expression Patterns ◽  
Mouse Skin ◽  
Exponential Growth Phase ◽  
Wild Type ◽  
Subcutaneous Infection ◽  
Group A

ABSTRACT Group A Streptococcus (GAS) acquires mutations of the virulence regulator CovRS in human and mouse infections, and these mutations result in the upregulation of virulence genes and the downregulation of the protease SpeB. To identify in vivo mutants with novel phenotypes, GAS isolates from infected mice were screened by enzymatic assays for SpeB and the platelet-activating factor acetylhydrolase Sse, and a new type of variant that had enhanced Sse expression and normal levels of SpeB production was identified (the variants had a phenotype referred to as enhanced Sse activity [SseA+] and normal SpeB activity [SpeBA+]). SseA+ SpeBA+ variants had transcript levels of CovRS-controlled virulence genes comparable to those of a covS mutant but had no covRS mutations. Genome resequencing of an SseA+ SpeBA+ isolate identified a C605A nonsense mutation in orphan kinase gene rocA, and 6 other SseA+ SpeBA+ isolates also had nonsense mutations or small indels in rocA. RocA and CovS mutants had similar levels of enhancement of the expression of CovRS-controlled virulence genes at the exponential growth phase; however, mutations of RocA but not mutations of CovS did not result in the downregulation of speB transcription at stationary growth phase or in subcutaneous infection of mice. GAS with RocA and CovS mutations caused greater enhancement of the expression of hasA than spyCEP in mouse skin infection than wild-type GAS did. RocA mutants ranked between wild-type GAS and CovS mutants in skin invasion, inhibition of neutrophil recruitment, and virulence in subcutaneous infection of mice. Thus, GAS RocA mutants can be selected in subcutaneous infections in mice and exhibit gene expression patterns and virulences distinct from those of CovS mutants. The findings provide novel information for understanding GAS fitness mutations in vivo, virulence gene regulation, in vivo gene expression, and virulence.

scholarly journals The YAP1 Homolog–Mediated Oxidative Stress Tolerance Is Crucial for Pathogenicity of the Necrotrophic Fungus Alternaria alternata in Citrus

2009 ◽  
Vol 22 (8) ◽  
pp. 942-952 ◽  
Author(s):  
Ching-Hsuan Lin ◽  
Siwy Ling Yang ◽  
Kuang-Ren Chung
Keyword(s):  
Oxidative Stress ◽  
Alternaria Alternata ◽  
Critical Role ◽  
Disease Process ◽  
Brown Spot ◽  
Null Mutant ◽  
Wild Type ◽  
Protein Fusion ◽  
Fungal Pathogenicity

Citrus brown spot disease is caused by the necrotrophic fungus Alternaria alternata. Its pathogenic capability has been thought to depend exclusively on the production of host-selective ACT toxin. However, circumvention of plant defenses is also likely to be important for the disease process. To investigate the fungal response to host-generated reactive oxygen species (ROS), we cloned and characterized the AaAP1 gene of A. alternata, which encodes a polypeptide resembling yeast YAP1-like transcriptional activators implicated in cellular responses to stress. Expression of the AaAP1 gene in a wild-type strain was primarily induced by H2O2 or ROS-generating oxidants. Using a loss-of-function mutation in the AaAP1 gene, we demonstrated an essential requirement for oxidative tolerance during the host invasion step. Mutants lacking AaAP1 showed increased sensitivity to H2O2 and loss of fungal pathogenicity. The ΔAaAP1 null mutant did not cause any visible necrotic lesions on wounded or unwounded leaves of citrus cv. Minneola. Compared with the wild type, the null mutant displayed lower catalase, peroxidase, and superoxide dismutase activities. All mutant phenotypes were restored to the wild type in fungal strains expressing a functional copy of AaAP1. Upon exposure to H2O2, the AaAP1::sGFP (synthetic green fluorescent protein) fusion protein became localized in the nucleus. Inoculation of the mutant with NADPH oxidase inhibitors partially restored fungal pathogenicity. Our results highlight the global regulatory role of a YAP1 homolog in response to oxidative stress in A. alternata and provide insights into the critical role of ROS detoxification in the pathogenicity of A. alternata.

scholarly journals Mutations in the lrpE Gene of Ralstonia solanacearum Affects Hrp Pili Production and Virulence

2006 ◽  
Vol 19 (8) ◽  
pp. 884-895 ◽  
Author(s):  
Yukio Murata ◽  
Naoyuki Tamura ◽  
Kazuhiro Nakaho ◽  
Takafumi Mukaihara
Keyword(s):  
Cell Surface ◽  
Growth Phase ◽  
Ralstonia Solanacearum ◽  
Vascular System ◽  
Exponential Growth Phase ◽  
Bacterial Cells ◽  
Wild Type ◽  
Bacterial Surface ◽  
Bacterial Morphology ◽  
In The Wild

The Ralstonia solanacearum hrpB-regulated gene lrpE (hpx5/brg24) encodes a PopC-like leucine-rich repeat (LRR) protein that carries 11 tandem LRR in the central region. Defects in the lrpE gene slightly reduced the virulence of R. solanacearum on host plants and changed the bacterial morphology leading to the formation of large aggregates in a minimal medium. The aggregation in the ΔlrpE background required the presence of a functional Hrp type III secretion system. In wild-type R. solanacearum, Hrp pili disappeared from the bacterial surface at the end of the exponential growth phase, when the pili form into long bundles. However, even in the late growth phase, bundled Hrp pili were still observed on the cell surface of the ΔlrpE mutant. Such bundles were entangled and anchored the mutant cells in the aggregates. In contrast to PopC, LrpE accumulated in bacterial cells and did not translocate into plant cells as an effector protein. The expression levels of hrp genes increased three- to fivefold in the ΔlrpE background compared with those in the wild type. We propose that LrpE may negatively regulate the production of Hrp pili on the cell surface of R. solanacearum to disperse bacterial cells from aggregates. In turn, dispersal may contribute to the movement of the pathogen in the plant vascular system and, as a consequence, the pathogenicity of R. solanacearum.

scholarly journals Attenuation of Late-Stage Disease in Mice Infected bythe Mycobacterium tuberculosis Mutant Lacking theSigF Alternate Sigma Factor and Identification ofSigF-Dependent Genes by MicroarrayAnalysis

2004 ◽  
Vol 72 (3) ◽  
pp. 1733-1745 ◽  
Author(s):  
Deborah E. Geiman ◽  
Deepak Kaushal ◽  
Chiew Ko ◽  
Sandeep Tyagi ◽  
Yukari C. Manabe ◽  
...  
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Stationary Phase ◽  
Mutant Strain ◽  
Microarray Analysis ◽  
Growth Phase ◽  
Sigma Factor ◽  
Granulomatous Inflammation ◽  
Exponential Growth Phase ◽  
Histopathological Analysis ◽  
Wild Type

ABSTRACT The Mycobacterium tuberculosis alternate sigma factor, SigF, is expressed during stationary growth phase and under stress conditions in vitro. To better understand the function of SigF we studied the phenotype of the M. tuberculosis ΔsigF mutant in vivo during mouse infection, tested the mutant as a vaccine in rabbits, and evaluated the mutant's microarray expression profile in comparison with the wild type. In mice the growth rates of theΔ sigF mutant and wild-type strains were nearly identical during the first 8 weeks after infection. At 8 weeks, theΔ sigF mutant persisted in the lung, while the wild type continued growing through 20 weeks. Histopathological analysis showed that both wild-type and mutant strains had similar degrees of interstitial and granulomatous inflammation during the first 12 weeks of infection. However, from 12 to 20 weeks the mutant strain showed smaller and fewer lesions and less inflammation in the lungs and spleen. Intradermal vaccination of rabbits with the M. tuberculosis ΔsigF strain, followed by aerosol challenge, resulted in fewer tubercles than did intradermal M. bovis BCG vaccination. Complete genomic microarray analysis revealed that 187 genes were relatively underexpressed in the absence of SigF in early stationary phase, 277 in late stationary phase, and only 38 genes in exponential growth phase. Numerous regulatory genes and those involved in cell envelope synthesis were down-regulated in the absence of SigF; moreover, the ΔsigF mutant strain lacked neutral red staining, suggesting a reduction in the expression of envelope-associated sulfolipids. Examination of 5′-untranslated sequences among the downregulated genes revealed multiple instances of a putative SigF consensus recognition sequence: GGTTTCX18GGGTAT. These results indicate that in the mouse the M. tuberculosis ΔsigF mutant strain persists in the lung but at lower bacterial burdens than wild type and is attenuated by histopathologic assessment. Microarray analysis has identified SigF-dependent genes and a putative SigF consensus recognition site.

Construction of a [NiFe]-hydrogenase deletion mutant of Desulfovibrio vulgaris Hildenborough

2005 ◽  
Vol 33 (1) ◽  
pp. 59-60 ◽  
Author(s):  
A. Goenka ◽  
J.K. Voordouw ◽  
W. Lubitz ◽  
W. Gärtner ◽  
G. Voordouw
Keyword(s):  
Growth Phase ◽  
Exponential Growth ◽  
Deletion Mutant ◽  
Stationary Growth Phase ◽  
Exponential Growth Phase ◽  
Desulfovibrio Vulgaris ◽  
Wild Type ◽  
Stationary Growth ◽  
Desulfovibrio Vulgaris Hildenborough ◽  
Mutant Cells

A mutant of Desulfovibrio vulgaris Hildenborough lacking a gene for [NiFe] hydrogenase was generated. Growth studies, performed for the mutant in comparison with the wild-type, showed no strong differences during the exponential growth phase. However, the mutant cells died more rapidly in the stationary growth phase.

scholarly journals Importance of catalase in the adaptive response to hydrogen peroxide: analysis of acatalasaemic Saccharomyces cerevisiae

1996 ◽  
Vol 320 (1) ◽  
pp. 61-67 ◽  
Author(s):  
Shingo IZAWA ◽  
Yoshiharu INOUE ◽  
Akira KIMURA
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Adaptive Response ◽  
Yeast Cells ◽  
Exponential Growth Phase ◽  
Wild Type ◽  
Single Mutant ◽  
Mutant Cells ◽  
Similar Growth

Controversy about the importance of catalase in the detoxification of H2O2 in human erythrocytes continues. It has been suggested that catalase has no role in the clearance of H2O2 in erythrocytes. In the present study we investigated the role of catalase in the defence mechanism against oxidative stress using Saccharomyces cerevisiae. S. cerevisiae has two catalases, catalase A and catalase T. We constructed a double mutant (acatalasaemic mutant) unable to produce either catalase A or catalase T, and compared it with wild-type and single-mutant cells. The acatalasaemic mutant cells showed a similar growth rate to wild-type cells under non-oxidative stress conditions, and showed a similar susceptibility to H2O2 stress in the exponential growth phase. The acatalasaemic mutant cells at stationary phase were, however, much more sensitive to H2O2 stress than wild-type and single-mutant cells. Moreover, the ability of acatalasaemic and single-mutant cells to show adaptation to 2 mM H2O2 was distinctly inferior to that of wild-type cells. These results suggest that catalase is not essential for yeast cells under normal conditions, but plays an important role in the acquisition of tolerance to oxidative stress in the adaptive response of these cells.

Sélection et analyse de mutants thermotolérants de Zymomonas mobilis, producteurs d'éthanol

1985 ◽  
Vol 31 (10) ◽  
pp. 934-937 ◽  
Author(s):  
Bénédicte Berthelin ◽  
Joseph Zucca ◽  
Jean-François Mescle
Keyword(s):  
Ethanol Production ◽  
Growth Kinetics ◽  
Growth Phase ◽  
Exponential Growth ◽  
Type Strain ◽  
Zymomonas Mobilis ◽  
Wild Type Strain ◽  
Exponential Growth Phase ◽  
Wild Type ◽  
Mutant Strains

Mutagenesis of Zymomonas mobilis ATCC 10988 induced by nitrosoguanidine and ethyl methanesulfonate leads to the acquisition of thermotolerant character. The nitrosoguanidine allows the obtention of the best mutants. At 38 °C, these mutant strains have growth kinetics and ethanol production rates similar to those of the wild-type strain grown at 30 °C. The mutants show delayed ethanol production when compared with Zymomonas mobilis ATCC 10988: this production occurs in part during the exponential growth phase and is still active at the beginning of the stationary phase.

scholarly journals The Ccr4-Not Complex Regulates Skn7 through Srb10 Kinase

2007 ◽  
Vol 6 (12) ◽  
pp. 2251-2259 ◽  
Author(s):  
Eve Lenssen ◽  
Nowel Azzouz ◽  
Agnès Michel ◽  
Emilie Landrieux ◽  
Martine A. Collart
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Critical Role ◽  
Mrna Degradation ◽  
Dependent Manner ◽  
Wild Type ◽  
Cellular Events ◽  
Protein Ubiquitination ◽  
And Oxidative Stress ◽  
Two Hybrid

ABSTRACT The Ccr4-Not complex is a multifunctional regulatory platform composed of nine subunits that controls diverse cellular events including mRNA degradation, protein ubiquitination, and transcription. In this study, we identified the yeast Saccharomyces cerevisiae osmotic and oxidative stress transcription factor Skn7 as a new target for regulation by the Ccr4-Not complex. Skn7 interacts with Not1 in a two-hybrid assay and coimmunoprecipitates with Not5 in a Not4-dependent manner. Skn7-dependent expression of OCH1 and Skn7 binding to the OCH1 promoter are increased in not4Δ or not5Δ mutants. Skn7 purified from wild-type cells but not from not4Δ cells is associated with the Srb10 kinase. This kinase plays a central role in the regulation of Skn7 by Not4, since increased OCH1 expression in not4Δ cells requires Srb10. These results reveal a critical role for the Ccr4-Not complex in the mechanism of activation of Skn7 that is dependent upon the Srb10 kinase.

scholarly journals Gingipain RgpB Is Excreted as a Proenzyme in the vimA-Defective Mutant Porphyromonas gingivalis FLL92

2003 ◽  
Vol 71 (7) ◽  
pp. 3740-3747 ◽  
Author(s):  
G. Jon Olango ◽  
Francis Roy ◽  
Shaun M. Sheets ◽  
Mary K. Young ◽  
Hansel M. Fletcher
Keyword(s):  
Growth Phase ◽  
Protease Activity ◽  
Posttranscriptional Regulation ◽  
Type Strain ◽  
Wild Type Strain ◽  
Exponential Growth Phase ◽  
Wild Type ◽  
Defective Mutant ◽  
Inactive Form

ABSTRACT We have previously shown that the unique vimA (virulence-modulating) gene could modulate proteolytic activity in Porphyromomas gingivalis. Although a reduction in cysteine protease activity was observed in the vimA-defective mutant, P. gingivalis FLL92, compared to that of the wild-type strain, no changes were seen in the expression of the gingipain genes. This result might suggest posttranscriptional regulation of protease expression. To determine whether there was a defect in the translation, transport, or maturation of the gingipains, P. gingivalis FLL92 was further characterized. In contrast to the wild-type strain, a 90% reduction was seen in both Rgp and Kgp protease activities in strain FLL92 during the exponential growth phase. These activities, however, increased to approximately 60% of that of the wild-type strain during stationary phase. Throughout all the growth phases, Rgp and Kgp activities were mostly soluble, in contrast to those of the wild-type strain. Western blot analyses identified unique Rgp- and Kgp-immunoreactive bands in extracellular protein fractions from FLL92 grown to late exponential phase. Also, the RgpB proenzyme was identified in this fraction by mass spectrometry. In addition, in vitro protease activity could be induced by a urea denaturation-renaturation cycle in this fraction. These results indicate that protease activity in P. gingivalis may be growth phase regulated, possibly by multiple mechanisms. Furthermore, the gingipain RgpB is excreted in an inactive form in the vimA mutant. In addition, these results provide the first evidence of posttranslational regulation of protease activity in P. gingivalis and may suggest an important role for the vimA gene in protease activation in this organism.

Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling

2007 ◽  
Vol 293 (4) ◽  
pp. H2101-H2108 ◽  
Author(s):  
Meijing Wang ◽  
Wenjun Zhang ◽  
Paul Crisostomo ◽  
Troy Markel ◽  
Kirstan K. Meldrum ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cell ◽  
Myocardial Function ◽  
Critical Role ◽  
Caspase 8 ◽  
Biological Processes ◽  
Signal Transducer ◽  
Wild Type ◽  
Mapk Activation ◽  
Isolated Hearts

Signal transducer and activator of transcription (STAT) 3 is involved in mediating a broad range of biological processes, including cell survival, proliferation, and immune response. Recent evidence has indicated that STAT3 in cardiomyocytes can be activated by ischemic-oxidative stress and exerts cardioprotection in the ischemic heart. There is no information, however, regarding the effect of endothelial cell-derived STAT3 on the myocardial response to ischemiareperfusion (I/R) injury. We hypothesized that the ablation of the STAT3 gene in endothelial cells would worsen postischemic myocardial function by affecting capillary network integrity, suppressing antiapoptotic signaling. Isolated hearts from wild-type and endothelial cell STAT3 knockout (STAT3KO) mice were subjected to 20 min of global ischemia followed by 60 min of reperfusion. Endothelial cell STAT3 deficiency decreased recovery of myocardial function in response to I/R, which was associated with higher levels of LDH release, decreased activation of myocardial STAT3, and elevated p38 MAPK activation in STAT3 endothelial knockout (KO) hearts. In addition, although no significant apoptosis was observed in wild-type and KO hearts, our results showed more expression of myocardial caspase-8 and more apoptosis in the myocardium around the capillary in STAT3KO mice subjected to I/R. Furthermore, endothelial cell STAT3 ablation resulted in increased myocardial expression of IL-6 and suppressor of cytokine signal 3. This study demonstrates that endothelial cell-derived STAT3 plays an important role in postischemic myocardial function.

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