scholarly journals Trichoderma atroviride Transcriptional Regulator Xyr1 Supports the Induction of Systemic Resistance in Plants

2014 ◽  
Vol 80 (17) ◽  
pp. 5274-5281 ◽  
Author(s):  
Barbara Reithner ◽  
Astrid R. Mach-Aigner ◽  
Alfredo Herrera-Estrella ◽  
Robert L. Mach
Keyword(s):  
Regulatory Protein ◽  
Transcriptional Regulator ◽  
Systemic Resistance ◽  
Accessory Cell ◽  
Transcript Analysis ◽  
Trichoderma Atroviride ◽  
Cell Wall Degrading Enzymes ◽  
Content Type ◽  
Precise Role

ABSTRACTAs a result of a transcriptome-wide analysis of the ascomyceteTrichoderma atroviride, mycoparasitism-related genes were identified; of these, 13 genes were further investigated for differential expression.In silicoanalysis of the upstream regulatory regions of these genes pointed to xylanase regulator 1 (Xyr1) as a putatively involved regulatory protein. Transcript analysis of thexyr1gene ofT. atroviridein confrontation with other fungi allowed us to determine thatxyr1levels increased during mycoparasitism. To gain knowledge about the precise role of Xyr1 in the mycoparasitic process, the corresponding gene was deleted from theT. atroviridegenome. This resulted in strong reductions in the transcript levels ofaxe1andswo1, which encode accessory cell wall-degrading enzymes considered relevant for mycoparasitism. We also analyzed the role of Xyr1 in theTrichoderma-Arabidopsisinteraction, finding that the plant response elicited byT. atrovirideis delayed if Xyr1 is missing in the fungus.

scholarly journals Mutation ofRv2887, amarR-Like Gene, Confers Mycobacterium tuberculosis Resistance to an Imidazopyridine-Based Agent

2015 ◽  
Vol 59 (11) ◽  
pp. 6873-6881 ◽  
Author(s):  
Kathryn Winglee ◽  
Shichun Lun ◽  
Marco Pieroni ◽  
Alan Kozikowski ◽  
William Bishai
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Drug Targets ◽  
Efflux Pump ◽  
Transcriptional Regulator ◽  
Cross Resistance ◽  
Loss Of Function ◽  
Strong Activity ◽  
Content Type ◽  
Novel Drug

ABSTRACTDrug resistance is a major problem inMycobacterium tuberculosiscontrol, and it is critical to identify novel drug targets and new antimycobacterial compounds. We have previously identified an imidazo[1,2-a]pyridine-4-carbonitrile-based agent, MP-III-71, with strong activity againstM. tuberculosis. In this study, we evaluated mechanisms of resistance to MP-III-71. We derived three independentM. tuberculosismutants resistant to MP-III-71 and conducted whole-genome sequencing of these mutants. Loss-of-function mutations inRv2887were common to all three MP-III-71-resistant mutants, and we confirmed the role ofRv2887as a gene required for MP-III-71 susceptibility using complementation. The Rv2887 protein was previously unannotated, but domain and homology analyses suggested it to be a transcriptional regulator in the MarR (multiple antibiotic resistance repressor) family, a group of proteins first identified inEscherichia colito negatively regulate efflux pumps and other mechanisms of multidrug resistance. We found that two efflux pump inhibitors, verapamil and chlorpromazine, potentiate the action of MP-III-71 and that mutation ofRv2887abrogates their activity. We also used transcriptome sequencing (RNA-seq) to identify genes which are differentially expressed in the presence and absence of a functional Rv2887 protein. We found that genes involved in benzoquinone and menaquinone biosynthesis were repressed by functional Rv2887. Thus, inactivating mutations ofRv2887, encoding a putative MarR-like transcriptional regulator, confer resistance to MP-III-71, an effective antimycobacterial compound that shows no cross-resistance to existing antituberculosis drugs. The mechanism of resistance ofM. tuberculosisRv2887mutants may involve efflux pump upregulation and also drug methylation.

scholarly journals The Global Transcription Factor Lrp Controls Virulence Modulation in Xenorhabdus nematophila

2015 ◽  
Vol 197 (18) ◽  
pp. 3015-3025 ◽  
Author(s):  
Elizabeth A. Hussa ◽  
Ángel M. Casanova-Torres ◽  
Heidi Goodrich-Blair
Keyword(s):  
Transcription Factor ◽  
Phenotypic Variation ◽  
Pathogenic Bacteria ◽  
Regulatory Protein ◽  
Inverse Correlation ◽  
Xenorhabdus Nematophila ◽  
Insect Larvae ◽  
Content Type ◽  
Expression Levels

ABSTRACTThe bacteriumXenorhabdus nematophilaengages in phenotypic variation with respect to pathogenicity against insect larvae, yielding both virulent and attenuated subpopulations of cells from an isogenic culture. The global regulatory protein Lrp is necessary forX. nematophilavirulence and immunosuppression in insects, as well as colonization of the mutualistic host nematodeSteinernema carpocapsae, and mediates expression of numerous genes implicated in each of these phenotypes. Given the central role of Lrp inX. nematophilahost associations, as well as its involvement in regulating phenotypic variation pathways in other bacteria, we assessed its function in virulence modulation. We discovered that expression oflrpvaries within an isogenic population, in a manner that correlates with modulation of virulence. Unexpectedly, although Lrp is necessary for optimal virulence and immunosuppression, cells expressing high levels oflrpwere attenuated in these processes relative to those with low to intermediatelrpexpression. Furthermore, fixed expression oflrpat high and low levels resulted in attenuated and normal virulence and immunosuppression, respectively, and eliminated population variability of these phenotypes. These data suggest that fluctuatinglrpexpression levels are sufficient to drive phenotypic variation inX. nematophila.IMPORTANCEMany bacteria use cell-to-cell phenotypic variation, characterized by distinct phenotypic subpopulations within an isogenic population, to cope with environmental change. Pathogenic bacteria utilize this strategy to vary antigen or virulence factor expression. Our work establishes that the global transcription factor Lrp regulates phenotypic variation in the insect pathogenXenorhabdus nematophila, leading to attenuation of virulence and immunosuppression in insect hosts. Unexpectedly, we found an inverse correlation between Lrp expression levels and virulence: high levels of expression of Lrp-dependent putative virulence genes are detrimental for virulence but may have an adaptive advantage in other aspects of the life cycle. Investigation ofX. nematophilaphenotypic variation facilitates dissection of this phenomenon in the context of a naturally occurring symbiosis.

scholarly journals Novel Mutations Associated with Clofazimine Resistance inMycobacterium abscessus

2018 ◽  
Vol 62 (7) ◽  
Author(s):  
Yuanyuan Chen ◽  
Jiazhen Chen ◽  
Shuo Zhang ◽  
Wanliang Shi ◽  
Wenhong Zhang ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Regulatory Protein ◽  
Mycobacterium Abscessus ◽  
Pulmonary Infections ◽  
Mechanisms Of Resistance ◽  
Novel Mutations ◽  
Content Type ◽  
Future Studies ◽  
Transcriptional Regulatory

ABSTRACTMycobacterium abscessusis a major nontuberculous mycobacterial (NTM) pathogen and is responsible for about 80% of all pulmonary infections caused by rapidly growing mycobacteria. Clofazimine is an effective drug active againstM. abscessus, but the mechanism of resistance to clofazimine inM. abscessusis unknown. To investigate the molecular basis of clofazimine resistance inM. abscessus, we isolated 29M. abscessusmutants resistant to clofazimine and subjected them to whole-genome sequencing to identify possible mutations associated with clofazimine resistance. We found that mutations in the MAB_2299c gene (which encodes a possible transcriptional regulatory protein), MAB_1483, and MAB_0540 are most commonly associated with clofazimine resistance. In addition, mutations in MAB_0416c, MAB_4099c, MAB_2613, MAB_0409, and MAB_1426 were also associated with clofazimine resistance but less frequently. Two identical mutations which are likely to be polymorphisms unrelated to clofazimine resistance were found in MAB_4605c and MAB_4323 in 13 mutants. We conclude that mutations in MAB_2299c, MAB_1483, and MAB_0540 are the major mechanisms of clofazimine resistance inM. abscessus. Future studies are needed to address the role of the identified mutations in clofazimine resistance inM. abscessus. Our findings have implications for understanding mechanisms of resistance to clofazimine and for rapid detection of clofazimine resistance in this organism.

scholarly journals ThechbGGene of the Chitobiose (chb) Operon of Escherichia coli Encodes a Chitooligosaccharide Deacetylase

2012 ◽  
Vol 194 (18) ◽  
pp. 4959-4971 ◽  
Author(s):  
Subhash Chandra Verma ◽  
Subramony Mahadevan
Keyword(s):  
Escherichia Coli ◽  
Metal Binding ◽  
Inflammatory Diseases ◽  
Regulatory Protein ◽  
Loss Of Function ◽  
Content Type ◽  
Reading Frame ◽  
E Coli ◽  
Evolutionarily Conserved

ABSTRACTThechboperon ofEscherichia coliis involved in the utilization of the β-glucosides chitobiose and cellobiose. The function ofchbG(ydjC), the sixth open reading frame of the operon that codes for an evolutionarily conserved protein is unknown. We show thatchbGencodes a monodeacetylase that is essential for growth on the acetylated chitooligosaccharides chitobiose and chitotriose but is dispensable for growth on cellobiose and chitosan dimer, the deacetylated form of chitobiose. The predicted active site of the enzyme was validated by demonstrating loss of function upon substitution of its putative metal-binding residues that are conserved across the YdjC family of proteins. We show that activation of thechbpromoter by the regulatory protein ChbR is dependent on ChbG, suggesting that deacetylation of chitobiose-6-P and chitotriose-6-P is necessary for their recognition by ChbR as inducers. Strains carrying mutations inchbRconferring the ability to grow on both cellobiose and chitobiose are independent ofchbGfunction for induction, suggesting that gain of function mutations in ChbR allow it to recognize the acetylated form of the oligosaccharides. ChbR-independent expression of the permease and phospho-β-glucosidase from a heterologous promoter did not support growth on both chitobiose and chitotriose in the absence ofchbG, suggesting an additional role ofchbGin the hydrolysis of chitooligosaccharides. The homologs ofchbGin metazoans have been implicated in development and inflammatory diseases of the intestine, indicating that understanding the function ofE. colichbGhas a broader significance.

scholarly journals Properties and Biological Role of Streptococcal Fratricins

2012 ◽  
Vol 78 (10) ◽  
pp. 3515-3522 ◽  
Author(s):  
Kari Helene Berg ◽  
Truls Johan Biørnstad ◽  
Ola Johnsborg ◽  
Leiv Sigve Håvarstein
Keyword(s):  
Cell Wall ◽  
Genetic Transformation ◽  
Natural Transformation ◽  
Current View ◽  
Dna Uptake ◽  
Cell Wall Degrading Enzymes ◽  
Content Type ◽  
Streptococcal Species ◽  
Natural Genetic Transformation

ABSTRACTCompetence for natural genetic transformation is widespread in the genusStreptococcus. The current view is that all streptococcal species possess this property. In addition to the proteins required for DNA uptake and recombination, competent streptococci secrete muralytic enzymes termed fratricins. Since the synthesis and secretion of these cell wall-degrading enzymes are always coupled to competence development in streptococci, fratricins are believed to carry out an important function associated with natural transformation. This minireview summarizes what is known about the properties of fratricins and discusses their possible biological roles in streptococcal transformation.

scholarly journals Role of AxyZ Transcriptional Regulator in Overproduction of AxyXY-OprZ Multidrug Efflux System in Achromobacter Species Mutants Selected by Tobramycin

2017 ◽  
Vol 61 (8) ◽  
Author(s):  
Julien Bador ◽  
Catherine Neuwirth ◽  
Nadège Grangier ◽  
Marie Muniz ◽  
Leslie Germé ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Transcriptional Regulator ◽  
Multidrug Efflux ◽  
Efflux System ◽  
Aminoglycoside Resistance ◽  
Resistance Level ◽  
Content Type ◽  
Multidrug Efflux System

ABSTRACT AxyXY-OprZ is an RND-type efflux system that confers innate aminoglycoside resistance to Achromobacter spp. We investigated here a putative TetR family transcriptional regulator encoded by the axyZ gene located upstream of axyXY-oprZ. An in-frame axyZ gene deletion assay led to increased MICs of antibiotic substrates of the efflux system, including aminoglycosides, cefepime, fluoroquinolones, tetracyclines, and erythromycin, indicating that the product of axyZ negatively regulates expression of axyXY-oprZ. Moreover, we identified an amino acid substitution at position 29 of AxyZ (V29G) in a clinical Achromobacter strain that occurred during the course of chronic respiratory tract colonization in a cystic fibrosis (CF) patient. This substitution, also detected in three other strains exposed in vitro to tobramycin, led to an increase in the axyY transcription level (5- to 17-fold) together with an increase in antibiotic resistance level. This overproduction of AxyXY-OprZ is the first description of antibiotic resistance acquisition due to modification of a chromosomally encoded mechanism in Achromobacter and might have an impact on the management of infected CF patients. Indeed, tobramycin is widely used for aerosol therapy within this population, and we have demonstrated that it easily selects mutants with increased MICs of not only aminoglycosides but also fluoroquinolones, cefepime, and tetracyclines.

scholarly journals Role of GlnR in Controlling Expression of Nitrogen Metabolism Genes in Listeria monocytogenes

2020 ◽  
Vol 202 (19) ◽  
Author(s):  
Rajesh Biswas ◽  
Abraham L. Sonenshein ◽  
Boris R. Belitsky
Keyword(s):  
Listeria Monocytogenes ◽  
Nitrogen Metabolism ◽  
Transcriptional Regulator ◽  
Nitrogen Sources ◽  
Negative Regulator ◽  
Ammonium Uptake ◽  
Ammonium Transport ◽  
Growth Media ◽  
Content Type

ABSTRACT Listeria monocytogenes is a fastidious bacterial pathogen that can utilize only a limited number of nitrogen sources for growth. Both glutamine and ammonium are common nitrogen sources used in listerial defined growth media, but little is known about the regulation of their uptake or utilization. The functional role of L. monocytogenes GlnR, the transcriptional regulator of nitrogen metabolism genes in low-G+C Gram-positive bacteria, was determined using transcriptome sequencing and real-time reverse transcription-PCR experiments. The GlnR regulon included transcriptional units involved in ammonium transport (amtB glnK) and biosynthesis of glutamine (glnRA) and glutamate (gdhA) from ammonium. As in other bacteria, GlnR proved to be an autoregulatory repressor of the glnRA operon. Unexpectedly, GlnR was most active during growth with ammonium as the nitrogen source and less active in the glutamine medium, apparently because listerial cells perceive growth with glutamine as a nitrogen-limiting condition. Therefore, paradoxically, expression of the glnA gene, encoding glutamine synthetase, was highest in the glutamine medium. For the amtB glnK operon, GlnR served as both a negative regulator in the presence of ammonium and a positive regulator in the glutamine medium. The gdhA gene was subject to a third mode of regulation that apparently required an elevated level of GlnR for repression. Finally, activity of glutamate dehydrogenase encoded by the gdhA gene appeared to correlate inversely with expression of gltAB, the operon that encodes the other major glutamate-synthesizing enzyme, glutamate synthase. Both gdhA and amtB were also regulated, in a negative manner, by the global transcriptional regulator CodY. IMPORTANCE L. monocytogenes is a widespread foodborne pathogen. Nitrogen-containing compounds, such as the glutamate-containing tripeptide, glutathione, and glutamine, have been shown to be important for expression of L. monocytogenes virulence genes. In this work, we showed that a transcriptional regulator, GlnR, controls expression of critical listerial genes of nitrogen metabolism that are involved in ammonium uptake and biosynthesis of glutamine and glutamate. A different mode of GlnR-mediated regulation was found for each of these three pathways.

scholarly journals TheClostridium difficile spo0AGene Is a Persistence and Transmission Factor

2012 ◽  
Vol 80 (8) ◽  
pp. 2704-2711 ◽  
Author(s):  
Laura J. Deakin ◽  
Simon Clare ◽  
Robert P. Fagan ◽  
Lisa F. Dawson ◽  
Derek J. Pickard ◽  
...  
Keyword(s):  
Health Care ◽  
Clostridium Difficile ◽  
Murine Model ◽  
Persistent Infection ◽  
Transcriptional Regulator ◽  
Transmission Factor ◽  
Content Type ◽  
Antibiotic Associated Diarrhea ◽  
Significant Health

ABSTRACTClostridium difficileis a major cause of chronic antibiotic-associated diarrhea and a significant health care-associated pathogen that forms highly resistant and infectious spores. Spo0A is a highly conserved transcriptional regulator that plays a key role in initiating sporulation inBacillusandClostridiumspecies. Here, we use a murine model to study the role of theC. difficile spo0Agene during infection and transmission. We demonstrate thatC. difficile spo0Amutant derivatives can cause intestinal disease but are unable to persist within and effectively transmit between mice. Thus, theC. difficileSpo0A protein plays a key role in persistent infection, including recurrence and host-to-host transmission in mice.

scholarly journals Trichoderma atroviridefrom Predator to Prey: Role of the Mitogen-Activated Protein Kinase Tmk3 in Fungal Chemical Defense against Fungivory byDrosophila melanogasterLarvae

2018 ◽  
Vol 85 (2) ◽  
Author(s):  
Karina Atriztán-Hernández ◽  
Abigail Moreno-Pedraza ◽  
Robert Winkler ◽  
Therese Markow ◽  
Alfredo Herrera-Estrella
Keyword(s):  
Protein Kinase ◽  
Secondary Metabolite ◽  
Asexual Reproduction ◽  
Defense Mechanism ◽  
Mitogen Activated Protein Kinase ◽  
Trichoderma Atroviride ◽  
Content Type ◽  
Metabolite Production ◽  
Mitogen Activated Protein

ABSTRACTThe response to injury represents an important strategy for animals and plants to survive mechanical damage and predation. Plants respond to injury by activating a defense response that includes the production of an important variety of compounds that help them withstand predator attack and recover from mechanical injury (MI). Similarly, the filamentous fungusTrichoderma atrovirideresponds to MI by strongly modifying its transcriptional profile and producing asexual reproduction structures (conidia). Here, we analyzed whether the response to MI inT. atrovirideis related to a possible predator defense mechanism from a metabolic perspective. We found that the production of specific groups of secondary metabolites increases in response to MI but is reduced after fungivory byDrosophila melanogasterlarvae. We further show that fungivory results in repression of the expression of genes putatively involved in the regulation of secondary metabolite production inT. atroviride. Activation of secondary metabolite production appears to depend on the mitogen-activated protein kinase (MAPK) Tmk3. Interestingly,D. melanogasterlarvae preferred to feed on atmk3gene replacement mutant rather than on the wild-type strain. Consumption of the mutant strain, however, resulted in increased larval mortality.IMPORTANCEFungi, like other organisms, have natural predators, including fungivorous nematodes and arthropods that use them as an important food source. Thus, they require mechanisms to detect and respond to injury.Trichoderma atrovirideresponds to mycelial injury by rapidly regenerating its hyphae and developing asexual reproduction structures. Whether this injury response is associated with attack by fungivorous insects is unknown. Therefore, determining the possible conservation of a defense mechanism to predation inT. atrovirideand plants and elucidating the mechanisms involved in the establishment of this response is of major interest. Here, we describe the chemical response ofT. atrovirideto mechanical injury and fungivory and the role of a MAPK pathway in the regulation of this response.

scholarly journals LacR Is a Repressor oflacABCDand LacT Is an Activator oflacTFEG, Constituting thelacGene Cluster in Streptococcus pneumoniae

2014 ◽  
Vol 80 (17) ◽  
pp. 5349-5358 ◽  
Author(s):  
Muhammad Afzal ◽  
Sulman Shafeeq ◽  
Oscar P. Kuipers
Keyword(s):  
Streptococcus Pneumoniae ◽  
Carbon Source ◽  
Gene Cluster ◽  
Sole Carbon Source ◽  
Transcriptional Repressor ◽  
Transcriptional Regulator ◽  
Transcriptional Activator ◽  
Content Type ◽  
Elevated Expression

ABSTRACTComparison of the transcriptome ofStreptococcus pneumoniaestrain D39 grown in the presence of either lactose or galactose with that of the strain grown in the presence of glucose revealed the elevated expression of various genes and operons, including thelacgene cluster, which is organized into two operons, i.e.,lacoperon I (lacABCD) andlacoperon II (lacTFEG). Deletion of the DeoR family transcriptional regulatorlacRthat is present downstream of thelacgene cluster revealed elevated expression oflacoperon I even in the absence of lactose. This suggests a function of LacR as a transcriptional repressor oflacoperon I, which encodes enzymes involved in the phosphorylated tagatose pathway in the absence of lactose or galactose. Deletion oflacRdid not affect the expression oflacoperon II, which encodes a lactose-specific phosphotransferase. This finding was further confirmed by β-galactosidase assays with PlacA-lacZand PlacT-lacZin the presence of either lactose or glucose as the sole carbon source in the medium. This suggests the involvement of another transcriptional regulator in the regulation oflacoperon II, which is the BglG-family transcriptional antiterminator LacT. We demonstrate the role of LacT as a transcriptional activator oflacoperon II in the presence of lactose and CcpA-independent regulation of thelacgene cluster inS. pneumoniae.

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