scholarly journals The Endochitinase of Clonostachysrosea Expression in Bacillus amyloliquefaciens Enhances the Botrytis cinerea Resistance of Tomato

2018 ◽  
Vol 19 (8) ◽  
pp. 2221 ◽  
Author(s):  
Yangyang Zheng ◽  
Xudong Wang ◽  
Siyuan Liu ◽  
Kewei Zhang ◽  
Zhibo Cai ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Botrytis Cinerea ◽  
Molecular Mechanism ◽  
Bacillus Amyloliquefaciens ◽  
Chitinase Activity ◽  
Wild Type ◽  
Tomato Plants ◽  
Significant Difference ◽  
In The Wild ◽  
Related Enzyme

To investigate whether the ech42 gene in Clonostachysrosea can improve the biocontrol efficacy of Bacillus amyloliquefaciens and its molecular mechanism. Compared to the wild type, the B. amyloliquefaciens transformed with the ech42 gene exhibited higher chitinase activity. The B. amyloliquefaciens-ech42 also showed significantly higher biocontrol efficiency compared to Botrytiscinerea when tomato plants were pre-treated with B. amyloliquefaciens-ech42. No significant difference in biocontrol efficiency was observed between the wild type and B.amyloliquefaciens-ech42 when tomato plants were first infected by Botrytiscinerea. In addition, the activity of the defense-related enzyme polyphenol oxidase, but not superoxide dismutase, was significantly higher in B. amyloliquefaciens-ech42 than in the wild type. The ech42 enhances the biocontrol efficiency of B.amyloliquefaciens by increasing the capacity of preventative/curative effects in plants, rather than by killing the pathogens.

scholarly journals The Endochitinase of Clonostachys Rosea Enhances the Biocontrol Efficiency of Bacillus Amyloliquefaciens by Increasing Its Activities of Defense Enzymes

2018 ◽  
Author(s):  
Yangyang Zheng ◽  
Xudong Wang ◽  
Siyuan Liu ◽  
Kewei Zhang ◽  
Zhibo Cai ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Bacillus Amyloliquefaciens ◽  
Chitinase Activity ◽  
Defense Enzymes ◽  
Wild Type ◽  
Clonostachys Rosea ◽  
Tomato Plants ◽  
Significant Difference ◽  
In The Wild ◽  
Related Enzyme

To investigate whether the ech42 gene in Clonostachys rosea can improve the biocontrol efficacy of Bacillus amyloliquefaciens and its molecular mechanism.Compared to the wild type, the B. amyloliquefaciens transformed with the ech42 gene exhibited a higher chitinase activity. The B. amyloliquefaciens-ech42 also showed a significantly higher biocontrol efficiency against B. cinerea when tomato plants were pre-treated with amyloliquefaciens-ech42. No significant difference of control efficiency was observed between the wild type and amyloliquefaciens-ech42 when tomato plants were first infected by B. cinerea. In addition, the activity of the defense-related enzyme polyphenol oxidase, but not superoxide dismutase was significantly higher in amyloliquefaciens-ech42 than in the wild type.The ech42 enhances the Bacillus amyloliquefaciens biocontrol efficiency by increasing the capacity of protection/prevention to plants, rather treating/killing the pathogens.

scholarly journals Autoproteolysis of YscU of Yersinia pseudotuberculosis Is Important for Regulation of Expression and Secretion of Yop Proteins

2009 ◽  
Vol 191 (13) ◽  
pp. 4259-4267 ◽  
Author(s):  
Ann-Catrin Björnfot ◽  
Moa Lavander ◽  
Åke Forsberg ◽  
Hans Wolf-Watz
Keyword(s):  
Type Iii Secretion ◽  
Calcium Concentration ◽  
Wild Type Strain ◽  
Yersinia Pseudotuberculosis ◽  
Secretion System ◽  
Wild Type ◽  
Regulation Of Expression ◽  
Significant Difference ◽  
In The Wild ◽  
Needle Protein

ABSTRACT YscU of Yersinia can be autoproteolysed to generate a 10-kDa C-terminal polypeptide designated YscUCC. Autoproteolysis occurs at the conserved N↓PTH motif of YscU. The specific in-cis-generated point mutants N263A and P264A were found to be defective in proteolysis. Both mutants expressed and secreted Yop proteins (Yops) in calcium-containing medium (+Ca2+ conditions) and calcium-depleted medium (−Ca2+ conditions). The level of Yop and LcrV secretion by the N263A mutant was about 20% that of the wild-type strain, but there was no significant difference in the ratio of the different secreted Yops, including LcrV. The N263A mutant secreted LcrQ regardless of the calcium concentration in the medium, corroborating the observation that Yops were expressed and secreted in Ca2+-containing medium by the mutant. YscF, the type III secretion system (T3SS) needle protein, was secreted at elevated levels by the mutant compared to the wild type when bacteria were grown under +Ca2+ conditions. YscF secretion was induced in the mutant, as well as in the wild type, when the bacteria were incubated under −Ca2+ conditions, although the mutant secreted smaller amounts of YscF. The N263A mutant was cytotoxic for HeLa cells, demonstrating that the T3SS-mediated delivery of effectors was functional. We suggest that YscU blocks Yop release and that autoproteolysis is required to relieve this block.

scholarly journals Comparison of defence responses to Botrytis cinerea infection in tomato plants propagated in vitro and grown in vivo

2013 ◽  
Vol 49 (1-2) ◽  
pp. 115-121 ◽  
Author(s):  
Jacek Patykowski ◽  
Elżbieta Kuźniak ◽  
Henryk Urbaniak
Keyword(s):  
Superoxide Dismutase ◽  
Botrytis Cinerea ◽  
Ascorbate Peroxidase ◽  
Guaiacol Peroxidase ◽  
Activity Increase ◽  
Tomato Plants ◽  
Defence Responses ◽  
Defence Reactions

Defence reactions: O<sub>2<sub> - generation, superoxide dismutase, catalase, guaiacol peroxidase and ascorbate peroxidase activities after <em>B. cinerea</em> infection in tomato plants propagated <em>in vitro</em> and grown <em>in vivo</em> have been compared. Infection resulted in rapid O<sub>2<sub> - generation. Superoxide dismutase activity increase was slower than O<sub>2<sub> - response. In plants propagated <em>in vitro</em> catalase and guaiacol peroxidase activities after infection were induced less strongly than in plants grown <em>in vivo</em>. K<sub>2<sub>HPO<sub>4<sub> pretreatment of plants grown <em>in vitro</em> enhanced significantly the activities of catalase and guaiacol peroxidase after infection. Slight restriction of <em>B. cinerea</em> infection development in <em>in vitro</em> propagated plants pretreated with K<sub>2<sub>HP0<sub>4<sub> was observed.

The affinity of hemoglobin for oxygen affects ventilatory responses in mutant mice with Presbyterian hemoglobinopathy

2003 ◽  
Vol 285 (4) ◽  
pp. R747-R753 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Masakatsu Tamaki ◽  
Yo-ichi Suzuki ◽  
Michiko Iwase ◽  
Takuji Shirasawa ◽  
...  
Keyword(s):  
Minute Ventilation ◽  
Globin Gene ◽  
Open Circuit ◽  
Mutant Mice ◽  
Whole Body ◽  
Wild Type ◽  
Peripheral Tissues ◽  
Ventilatory Responses ◽  
Significant Difference ◽  
In The Wild

The purpose of this study was to test whether chronically enhanced O2 delivery to tissues, without arterial hyperoxia, can change acute ventilatory responses to hypercapnia and hypoxia. The effects of decreased hemoglobin (Hb)-O2 affinity on ventilatory responses during hypercapnia (0, 5, 7, and 9% CO2 in O2) and hypoxia (10 and 15% O2 in N2) were assessed in mutant mice expressing Hb Presbyterian (mutation in the β-globin gene, β108 Asn → Lys). O2 consumption during normoxia, measured via open-circuit methods, was significantly higher in the mutant mice than in wild-type mice. Respiratory measurements were conducted with a whole body, unrestrained, single-chamber plethysmograph under conscious conditions. During hypercapnia, there was no difference between the slopes of the hypercapnic ventilatory responses, whereas minute ventilation at the same levels of arterial PCO2 was lower in the Presbyterian mice than in the wild-type mice. During both hypoxic exposures, ventilatory responses were blunted in the mutant mice compared with responses in the wild-type mice. The effects of brief hyperoxia exposure (100% O2) after 10% hypoxia on ventilation were examined in anesthetized, spontaneously breathing mice with a double-chamber plethysmograph. No significant difference was found in ventilatory responses to brief hypoxia between both groups of mice, indicating possible involvement of central mechanisms in blunted ventilatory responses to hypoxia in Presbyterian mice. We conclude that chronically enhanced O2 delivery to peripheral tissues can reduce ventilation during acute hypercapnic and hypoxic exposures.

scholarly journals NADPH Oxidase Is Crucial for the Cellular Redox Homeostasis in Fungal Pathogen Botrytis cinerea

2019 ◽  
Vol 32 (11) ◽  
pp. 1508-1516
Author(s):  
Hua Li ◽  
Shiping Tian ◽  
Guozheng Qin
Keyword(s):  
Nadph Oxidase ◽  
Botrytis Cinerea ◽  
Fungal Pathogen ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Signal Transduction Pathway ◽  
Regulatory Subunit ◽  
Wild Type ◽  
Mutant Proteins ◽  
In The Wild

During interactions, both plants and pathogens produce reactive oxygen species (ROS). Plants generate ROS for defense induction, while pathogens synthesize ROS for growth, sporulation, and virulence. NADPH oxidase (NOX) complex in the plasma membrane represents a main protein complex for ROS production in pathogens. Although NOX plays a crucial role in pathogenicity of pathogens, the underlying molecular mechanisms of NOX, especially the proteins regulated by NOX, remain largely unknown. Here, we applied an iodoacetyl tandem mass tag-based redox proteomic assay to investigate the protein redox dynamics in deletion mutant of bcnoxR, which encodes a regulatory subunit of NOX in the fungal pathogen Botrytis cinerea. In total, 214 unique peptidyl cysteine (Cys) thiols from 168 proteins were identified and quantified in both the wild type and ∆bcnoxR mutant. The Cys thiols in the ∆bcnoxR mutant were generally more oxidized than those in the wild type, suggesting that BcNoxR is essential for maintaining the equilibrium of the redox state in B. cinerea. Site-specific thiol oxidation analysis indicated that 142 peptides containing the oxidized thiols changed abundance significantly in the ∆bcnoxR mutant. Proteins containing these differential peptides are classified into various functional categories. Functional analysis revealed that one of these proteins, 6-phosphate dehydrogenase, played roles in oxidative stress response and pathogenesis of B. cinerea. These results provide insight into the potential target proteins and the ROS signal transduction pathway regulated by NOX.

scholarly journals Transcriptome Analysis of Aspergillus nidulans Exposed to Camptothecin-Induced DNA Damage

2006 ◽  
Vol 5 (10) ◽  
pp. 1688-1704 ◽  
Author(s):  
Iran Malavazi ◽  
Marcela Savoldi ◽  
Sônia Marli Zingaretti Di Mauro ◽  
Carlos Frederico Martins Menck ◽  
Steven D. Harris ◽  
...  
Keyword(s):  
Dna Damage ◽  
Aspergillus Nidulans ◽  
Mutant Strain ◽  
Deletion Mutant ◽  
Time Course ◽  
Excision Repair ◽  
Wild Type ◽  
Significant Difference ◽  
Mutant Strains ◽  
In The Wild

ABSTRACT We have used an Aspergillus nidulans macroarray carrying sequences of 2,787 genes from this fungus to monitor gene expression of both wild-type and uvsB ATR (the homologue of the ATR gene) deletion mutant strains in a time course exposure to camptothecin (CPT). The results revealed a total of 1,512 and 1,700 genes in the wild-type and uvsB ATR deletion mutant strains that displayed a statistically significant difference at at least one experimental time point. We characterized six genes that have increased mRNA expression in the presence of CPT in the wild-type strain relative to the uvsB ATR mutant strain: fhdA (encoding a forkhead-associated domain protein), tprA (encoding a hypothetical protein that contains a tetratrico peptide repeat), mshA (encoding a MutS homologue involved in mismatch repair), phbA (encoding a prohibitin homologue), uvsC RAD51 (the homologue of the RAD51 gene), and cshA (encoding a homologue of the excision repair protein ERCC-6 [Cockayne's syndrome protein]). The induced transcript levels of these genes in the presence of CPT require uvsB ATR. These genes were deleted, and surprisingly, only the ΔuvsC mutant strain was sensitive to CPT; however, the others displayed sensitivity to a range of DNA-damaging and oxidative stress agents. These results indicate that the selected genes when inactivated display very complex and heterogeneous sensitivity behavior during growth in the presence of agents that directly or indirectly cause DNA damage. Moreover, with the exception of UvsC, deletion of each of these genes partially suppressed the sensitivity of the ΔuvsB strain to menadione and paraquat. Our results provide the first insight into the overall complexity of the response to DNA damage in filamentous fungi and suggest that multiple pathways may act in parallel to mediate DNA repair.

scholarly journals Hexanoic Acid-Induced Resistance Against Botrytis cinerea in Tomato Plants

2009 ◽  
Vol 22 (11) ◽  
pp. 1455-1465 ◽  
Author(s):  
Begonya Vicedo ◽  
Víctor Flors ◽  
María de la O Leyva ◽  
Ivan Finiti ◽  
Zhana Kravchuk ◽  
...  
Keyword(s):  
Botrytis Cinerea ◽  
Induced Resistance ◽  
Pseudomonas Syringae ◽  
Hexanoic Acid ◽  
Dependent Manner ◽  
Deficient Mutant ◽  
Callose Deposition ◽  
Tomato Plants ◽  
In The Wild ◽  
Ja Signaling

We have demonstrated that root treatment with hexanoic acid protects tomato plants against Botrytis cinerea. Hexanoic acid-induced resistance (Hx-IR) was blocked in the jasmonic acid (JA)-insensitive mutant jai1 (a coi1 homolog) and in the abscisic acid (ABA)-deficient mutant flacca (flc). Upon infection, the LoxD gene as well as the oxylipin 12-oxo-phytodienoic acid and the bioactive molecule JA-Ile were clearly induced in treated plants. However, the basal ABA levels were not altered. Hexanoic acid primed callose deposition against B. cinerea in a cultivar-dependent manner. Treated plants from Ailsa Craig, Moneymaker, and Rheinlands Ruhm showed increased callose deposition but not from Castlemart. Hexanoic acid did not prime callose accumulation in flc plants upon B. cinerea infection; therefore, ABA could act as a positive regulator of Hx-IR by enhancing callose deposition. Furthermore, although hexanoic acid protected the JA-deficient mutant defensless1 (def1), the priming for callose was higher than in the wild type. This suggests a link between JA and callose deposition in tomato. Hence, the obtained results support the idea that callose, oxylipins, and the JA-signaling pathway are involved in Hx-IR against B. cinerea. Moreover our data support the relevance of JA-signaling for basal defense against this necrotroph in tomato. Hexanoic acid also protected against Pseudomonas syringae, indicating a broad-spectrum effect for this new inducer.

scholarly journals Use of Selenate-Resistant Strains as Markers for the Spread and Survival of Botrytis cinerea Under Greenhouse Conditions

2006 ◽  
Vol 96 (11) ◽  
pp. 1195-1203 ◽  
Author(s):  
N. Korolev ◽  
T. Katan ◽  
Y. Elad
Keyword(s):  
Botrytis Cinerea ◽  
Plant Tissue ◽  
Fungicide Resistance ◽  
Total Population ◽  
Warm Season ◽  
Type B ◽  
Wild Type ◽  
Plant Debris ◽  
Significant Difference ◽  
Resistant Strains

Botrytis cinerea marked strains combining traits of fungicide resistance or sensitivity (carbendazim, iprodione) with resistance to selenate were created and assessed for use in studying the dispersal of B. cinerea and its survival inside plant tissue under greenhouse conditions. Marked strains differed in their ability to cause lesions and to disperse in the greenhouse. A strain that was the most aggressive in infecting plants was also the most successful in spreading across the greenhouse. Following 7 to 14 days of exposure to marked inoculum, about 90% of plants showed quiescent B. cinerea infection with no significant difference between hosts or seasons. However, in a warm season, most of the plants were infected with wild-type B. cinerea, whereas most of the winter-recovered B. cinerea strains were of the marked phenotype, showing the importance of local inoculum from within the glasshouse in winter. The air of the greenhouse contained the same population of marked B. cinerea in warm and in cold periods, whereas the total population was significantly higher in summer. In the warm season, mycelium of B. cinerea inside plant debris lost viability within 3 to 4 months, whereas it stayed viable for 4 months in the winter (December to March) and started to lose viability in April.

Effects of FABP7 on functional recovery after spinal cord injury in adult mice

2019 ◽  
Vol 31 (2) ◽  
pp. 291-297 ◽  
Author(s):  
Nobuo Senbokuya ◽  
Hideyuki Yoshioka ◽  
Takashi Yagi ◽  
Yuji Owada ◽  
Hiroyuki Kinouchi
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Functional Recovery ◽  
Gene Knockout ◽  
Neuronal Injury ◽  
Wild Type ◽  
Fatty Acid Binding ◽  
Significant Difference ◽  
Cord Injury ◽  
In The Wild

OBJECTIVEElucidating the mechanisms of neuronal injury is crucial for the development of spinal cord injury (SCI) treatments. Brain-type fatty acid–binding protein 7 (FABP7) is expressed in the adult rodent brain, especially in astrocytes, and has been reported to play a role in astrocyte function in various types of brain damage; however, its role after SCI has not been well studied. In this study, the authors evaluated the expression change of FABP7 after SCI using a mouse spinal cord compression model and observed the effect of FABP7 gene knockout on neuronal damage and functional recovery after SCI.METHODSFemale FABP7 knockout (KO) mice with a C57BL/6 background and their respective wild-type littermates were subjected to SCI with a vascular clip. The expression of FABP7, neuronal injury, and functional recovery after SCI were analyzed in both groups of mice.RESULTSWestern blot analysis revealed upregulation of FABP7 in the wild-type mice, which reached its peak 14 days after SCI, with a significant difference in comparison to the control mice. Immunohistochemistry also showed upregulation of FABP7 at the same time points, mainly in proliferative astrocytes. The number of surviving ventral neurons in the FABP7-KO mice at 28 days after SCI was significantly lower than that observed in the wild-type mice. In addition, motor functional recovery in the FABP7-KO mice was significantly worse than that of the wild-type mice.CONCLUSIONSThe findings of this study indicate that FABP7 could have a neuroprotective role that might be associated with modulation of astrocytes after SCI. FABP7 could potentially be a therapeutic target in the treatment of SCI.

Sign in / Sign up

Export Citation Format

Share Document