Home About us Contact
|
Home About us Contact | ||
|
|
||
Infection Process (infection + process)
Selected AbstractsTobacco blue mould disease caused by Peronospora hyoscyami f. sp. tabacinaMOLECULAR PLANT PATHOLOGY, Issue 1 2010ORLANDO BORRÁS-HIDALGO SUMMARY Blue mould [Peronospora hyoscyami f. sp. tabacina (Adam) Skalicky 1964] is one of the most important foliar diseases of tobacco that causes significant losses in the Americas, south-eastern Europe and the Middle East. This review summarizes the current knowledge of the mechanisms employed by this oomycete pathogen to colonize its host, with emphasis on molecular aspects of pathogenicity. In addition, key biochemical and molecular mechanisms involved in tobacco resistance to blue mould are discussed. Taxonomy: Kingdom: Chromista (Straminipila); Phylum: Heterokontophyta; Class: Oomycete; Order: Peronosporales; Family: Peronosporaceae; Genus: Peronospora; Species: Peronospora hyoscyami f. sp. tabacina. Disease symptoms: The pathogen typically causes localized lesions on tobacco leaves that appear as single, or groups of, yellow spots that often coalesce to form light-brown necrotic areas. Some of the leaves exhibit grey to bluish downy mould on their lower surfaces. Diseased leaves can become twisted, such that the lower surfaces turn upwards. In such cases, the bluish colour of the diseased plants becomes quite conspicuous, especially under moist conditions when sporulation is abundant. Hence the name of the disease: tobacco blue mould. Infection process: The pathogen develops haustoria within plant cells that are thought to establish the transfer of nutrients from the host cell, and may also act in the delivery of effector proteins during infection. Resistance: Several defence responses have been reported to occur in the Nicotiana tabacum,P. hyoscyami f. sp. tabacina interaction. These include the induction of pathogenesis-related genes, and a correlated increase in the activities of typical pathogenesis-related proteins, such as peroxidases, chitinases, ,-1,3-glucanases and lipoxygenases. Systemic acquired resistance is one of the best characterized tobacco defence responses activated on pathogen infection. [source] Leaf, floret and seed infection of wheat by Pyrenophora semeniperdaPLANT PATHOLOGY, Issue 4 2003M. A. Campbell Infection processes of Pyrenophora semeniperda on seedling and adult wheat leaves and wheat ears were investigated. Almost 100% germination of conidia occurred on seedling leaves, compared with 20,30% on adult leaves. Appressoria formed over the anticlinal epidermal cell walls and haloes always accompanied infection. Sometimes papillae formed within the leaves as a resistance mechanism. Infection hyphae ramified through the intercellular spaces of the mesophyll resulting in cellular disruption. The infection processes on floral tissues were similar to those observed on leaves; however, no infection occurred on anther, stigmatic or stylar tissues. Infection of ovarian tissue occurred both with and without appressoria formation. Hyphae grew mainly in the epidermal layers and appeared unable to breach the integumental layer as no growth was observed in endosperm or embryo tissues. The optimum dew period temperature for conidial germination was 23·6°C, compared with 19·9°C for lesion development, 20·4°C for the production of infection structures on seedling leaves and 23·7°C for floret infection. Leaf disease development occurred in a logistic manner in response to dew period, with maximum infection observed after 21 h compared with > 48 h in seeds. An initial dark phase during the dew period was necessary for infection and temperature after the dew period had an effect, with significantly more numerous and larger lesions being formed at 15°C compared with 30°C. Seedling leaves were found to be more susceptible than older leaves, under both field and controlled environment conditions. Infection of wheat seeds following inoculation of ears, or after harvest burial of inoculated disease-free seeds, was demonstrated. In the latter, 3-week-old seedlings were slightly stunted, whereas older plants were unaffected. The apparent unimportance of this plant pathogen as a cause of leaf disease in relation to its poor adaptation to dew periods and dew period temperature is discussed, along with the importance of its seed borne characteristics. [source] Behavioural changes in Schistocerca gregaria following infection with a fungal pathogen: implications for susceptibility to predationECOLOGICAL ENTOMOLOGY, Issue 3 2001Steven Arthurs Summary 1. Field observations have indicated that infection of locusts and grasshoppers by the fungal entomopathogen Metarhizium anisopliae var. acridum may result in a substantial increase in the host's susceptibility to predation, before death is caused directly by the disease. 2. Laboratory experiments were conducted to examine how the behaviour of the desert locust Schistocerca gregaria Forskål changes following infection by M. anisopliae var. acridum to explore some potential mechanisms underlying this phenomenon. 3. In the first experiment, which involved monitoring general locust activity in small cages throughout the disease incubation period, infected locusts were observed to increase locomotion and bodily movement from 3 days after infection until death (average survival time of 11 days). There was some evidence of reduced feeding and mating behaviour following infection. 4. In a second experiment, locusts were exposed individually to a simulated predator attack and the initiation and strength of any escape responses were measured. Infected locusts were observed to have a reduced escape capability (both the propensity to escape and the strength of the response). In contrast to the relatively early changes in general activity observed in the first experiment, this was only apparent at the late stages of infection shortly before death. 5. Both an increase in movement and general apparency early in the infection process, and reduced escape capability late on, suggest mechanisms whereby the susceptibility of locusts and grasshoppers to predation might be enhanced following infection with M. anisopliae var. acridum. [source] Sclerotinia sclerotiorum: When "to be or not to be" a pathogen?FEMS MICROBIOLOGY LETTERS, Issue 2 2005Dwayne D. Hegedus Abstract Sclerotinia sclerotiorum is unusual among necrotrophic pathogens in its requirement for senescent tissues to establish an infection and to complete the life cycle. A model for the infection process has emerged whereby the pathogenic phase is bounded by saprophytic phases; the distinction being that the dead tissues in the latter are generated by the actions of the pathogen. Initial colonization of dead tissue provides nutrients for pathogen establishment and resources to infect healthy plant tissue. The early pathogenicity stage involves production of oxalic acid and the expression of cell wall degrading enzymes, such as specific isoforms of polygalacturonase (SSPG1) and protease (ASPS), at the expanding edge of the lesion. Such activities release small molecules (oligo-galacturonides and peptides) that serve to induce the expression of a second wave of degradative enzymes that collectively bring about the total dissolution of the plant tissue. Oxalic acid and other metabolites and enzymes suppress host defences during the pathogenic phase, while other components initiate host cell death responses leading to the formation of necrotic tissue. The pathogenic phase is followed by a second saprophytic phase, the transition to which is effected by declining cAMP levels as glucose becomes available and further hydrolytic enzyme synthesis is repressed. Low cAMP levels and an acidic environment generated by the secretion of oxalic acid promote sclerotial development and completion of the life cycle. This review brings together histological, biochemical and molecular information gathered over the past several decades to develop this tri-phasic model for infection. In several instances, studies with Botrytis species are drawn upon for supplemental and supportive evidence for this model. In this process, we attempt to outline how the interplay between glucose levels, cAMP and ambient pH serves to coordinate the transition between these phases and dictate the biochemical and developmental events that define them. [source] Ambient pH controls the expression of endopolygalacturonase genes in the necrotrophic fungus Sclerotinia sclerotiorumFEMS MICROBIOLOGY LETTERS, Issue 2 2003Pascale Cotton Abstract In the necrotrophic fungus Sclerotinia sclerotiorum, secretion of polygalacturonases (PGs) and decrease of the environmental pH via oxalic acid production are considered as the main pathogenicity determinants. In order to evaluate the relationship between these two aspects of the infection process, we analyzed the expression of the endoPG-encoding genes pg1,3. Transcription of pg1,3 was not carbon regulated but was strictly controlled by pH and highly favored in a narrow range of acidic pH. During plant infection, a pH gradient was established in relation to oxalic acid secretion. Transcripts of pg1,3 were localized to the zone of colonization of healthy tissues while transcripts of genes encoding other lytic enzymes were restricted to the more acidic zones of the infected tissues. Our results show that progressive acidification of the ambient medium by the fungus is a major strategy for the sequential expression of pathogenicity factors. [source] Listeria monocytogenes response regulators important for stress tolerance and pathogenesisFEMS MICROBIOLOGY LETTERS, Issue 1 2001Birgitte H. Kallipolitis Abstract Environmental sensing by two-component signal transduction systems is likely to play a role for growth and survival of Listeria monocytogenes both during transmission in food products and within a host organism. Two-component systems typically consist of a membrane-associated sensor histidine kinase and a gene regulatory protein, the response regulator (RR). We have identified seven putative RR genes in L. monocytogenes LO28 by PCR using degenerate oligonucleotide primers. By insertional inactivation we obtained data suggesting that three of the putative RRs contribute to the pathogenicity of L. monocytogenes in mice. Strikingly, the mutants that were attenuated in virulence also had a decreased ability to grow in the presence of various stress conditions potentially encountered in an infection process. Thus, our data point to a connection between the ability of the putative two-component systems to sense and respond to certain environmental stimuli, and the virulence of L. monocytogenes. [source] The Role of DNA Recombination in Herpes Simplex Virus DNA ReplicationIUBMB LIFE, Issue 8 2003Dianna Wilkinson Abstract In many organisms the processes of DNA replication and recombination are closely linked. For instance, in bacterial and eukaryotic systems, replication forks can become stalled or damaged, in many cases leading to the formation of double stranded breaks. Replication restart is an essential mechanism in which the recombination and repair machinery can be used to continue replication after such a catastrophic event. DNA viruses of bacteria such as lambda and T4 also rely heavily on DNA recombination to replicate their genomes and both viruses encode specialized gene products which are required for recombination-dependent replication. In this review, we examine the linkage between replication and recombination in the eukaryotic pathogen, Herpes Simplex Virus Type 1 (HSV-1). The evidence that recombination plays an intrinsic role in HSV-1 DNA replication and the infection process will be reviewed. We have recently demonstrated that HSV-1 encodes two proteins which may be analogous to the lambda phage recombination system, Red ,and ,. The HSV-1 alkaline nuclease, a 5' to 3' exonuclease, and ICP8, a single stranded DNA binding protein, can carry out strand annealing reactions similar to those carried out by the lambda Red system. In addition, evidence suggesting that host recombination proteins may also be important for HSV-1 replication will be reviewed. In summary, it is likely that HSV-1 infection will require both viral and cellular proteins which participate in various pathways of recombination and that recombination-dependent replication is essential for the efficient replication of viral genomes. IUBMB Life, 55: 451-458, 2003 [source] Pathogen fitness components and genotypes differ in their sensitivity to nutrient and temperature variation in a wild plant,pathogen associationJOURNAL OF EVOLUTIONARY BIOLOGY, Issue 6 2007A.-L. LAINE Abstract Understanding processes maintaining variation in pathogen life-history stages affecting infectivity and reproduction is a key challenge in evolutionary ecology. Models of host,parasite coevolution are based on the assumption that genetic variation for host,parasite interactions is a significant cause of variation in infection, and that variation in environmental conditions does not overwhelm the genetic basis. However, surprisingly little is known about the stability of genotype,genotype interactions under variable environmental conditions. Here, using a naturally occurring plant,pathogen interaction, I tested whether the two distinct aspects of the infection process , infectivity and transmission potential , vary over realistic nutrient and temperature gradients. I show that the initial pathogen infectivity and host resistance responses are robust over the environmental gradients. However, for compatible responses there were striking differences in how different pathogen life-history stages and host and pathogen genotypes responded to environmental variation. For some pathogen genotypes even slight changes in temperature arrested spore production, rendering the developing infection ineffectual. The response of pathogen genotypes to environmental gradients varied in magnitude and even direction, so that their rankings changed across the abiotic gradients. Hence, the variable environment of spatially structured host,parasite interactions may strongly influence the maintenance of polymorphism in pathogen life-history stages governing transmission, whereas evolutionary trajectories of infectivity may be unaffected by the surrounding environment. [source] Lipid Peroxidation and Antioxidant Activities Involved in Resistance Response against Downy Mildew in Opium PoppyJOURNAL OF PHYTOPATHOLOGY, Issue 2 2010Mukesh K. Dubey Abstract The aim of this study was to observe the lipid peroxidation (LP) of cell membranes and antioxidant systems in response to inoculation of Peronospora arborescens causing downy mildew (DM) in opium poppy. Contents of the LP product, malondialdehyde (MDA) and antioxidant glutathione (GSH) were determined in leaves of two opium poppy genotypes, Pps-1 (highly resistant to DM) and Jawahar-16 (highly susceptible to DM) at different time intervals after inoculation (12 h, 24 h, 48 h and 72 h). The provided GSH content corresponded to that of total non-protein sulfhydryl groups. In leaves of Jawahar-16, a significant decrease in concentration of GSH and a persistent increase in concentration of MDA were recorded after inoculation in comparison to leaves of control plants. The continuous decrease in GSH content contributed to damage of cell membranes leading to disease development in Jawahar-16. On the other hand in a resistant genotype (Pps-1), initially at 12 h after inoculation (hai) the level of GSH was found to be high, but a transient and highly significant decrease in content of GSH and increase in content of MDA was observed at 24 hai in comparison to control plants of same genotype and also in comparison to inoculated plants of susceptible genotype (Jawahar-16). These results indicate that generation of GSH and MDA is negatively correlated during the infection process as found in the case of DM-resistant genotype Pps-1 at 24hai, which also suggests an increased need by the host plant for oxidative stress, required for hypersensitive response mediated defense mechanism. [source] Puccinia romagnoliana Marie & Sacc.JOURNAL OF PHYTOPATHOLOGY, Issue 4-5 2002a Potential Bioherbicide Agent for Biocontrol of Purple Nutsedge (Cyperus rotundus L.) in Mulberry Abstract The ingress, infection process and disease development of Puccinia romagnoliana Marie & Sacc. on purple nutsedge (Cyperus rotundus L.) and its cross-infectivity to an economically important sericultural crop, mulberry (Morus alba L.) were investigated under a scanning electron microscope. The potential of P. romagnoliana as a biocontrol agent was also evaluated for the control of purple nutsedge under greenhouse conditions. Uredinia of P. romagnoliana were paraphysate that bore numerous pedicellate urediniospores, having echinulate spore wall. Urediniospores had 2,3 subequatorial germpores, which gave rise to germtubes. Germtubes were observed to orientate toward stomata and terminated in appressoria, through which infection pegs were formed that penetrated the leaf. Symptoms developed on leaves 10 days after inoculation. P. romagnoliana was highly pathogenic to purple nutsedge, which, when disease was severe, caused death of the shoots and reduced both number and vigour of the tubers. P. romagnoliana did not infect the main commercial crop, mulberry. Thus, the present study demonstrated the potential ofP. romagnoliana as a bioherbicide to control the purple nutsedge in mulberry fields. [source] Dual Role for Ethylene in Susceptibility of Tomato to Verticillium WiltJOURNAL OF PHYTOPATHOLOGY, Issue 7-8 2001M. M. Robison Abstract Ethylene has been observed to both inhibit and promote the symptoms of Verticillium wilt (caused by Verticillium dahliae) in tomato. To test the hypothesis that ethylene has different effects at different stages in the infection process, ethylene levels were manipulated in V. dahliae -infected tomato plants by the application of an ethylene synthesis inhibitor aminoethoxyvinylglycine (AVG) and/or ethylene's biosynthetic precursor 1-aminocyclopropane-1-carboxylate (ACC) and the effects on disease severity were examined. Statistically significant reductions in disease severity were consistently obtained for AVG-treated plants that had ACC added at the time of inoculation. A model is therefore proposed in which post-infection ethylene enhances Verticillium wilt development in tomato whereas its presence at the time of infection inhibits disease development. [source] Developmental regulation of the glyoxylate cycle in the human pathogen Penicillium marneffeiMOLECULAR MICROBIOLOGY, Issue 6 2006David Cánovas Summary Penicillium marneffei is a thermally dimorphic opportunistic human pathogen with a saprophytic filamentous hyphal form at 25°C and a pathogenic unicellular yeast form at 37°C. During infection. P. marneffei yeast cells exist intracellularly in macrophages. To cope with nutrient deprivation during the infection process, a number of pathogens employ the glyoxylate cycle to utilize fatty acids as carbon sources. The genes which constitute this pathway have been implicated in pathogenesis. To investigate acetate and fatty acid utilization, the acuD gene encoding a key glyoxylate cycle enzyme (isocitrate lyase) was cloned. The acuD gene is regulated by both carbon source and temperature in P. marneffei, being strongly induced at 37°C even in the presence of a repressing carbon source such as glucose. When introduced into the non-pathogenic monomorphic fungus Aspergillus nidulans, the P. marneffei acuD promoter only responds to carbon source. Similarly, when the A. nidulans acuD promoter is introduced into P. marneffei it only responds to carbon source suggesting that P. marneffei possesses both cis elements and trans -acting factors to control acuD by temperature. The Zn(II)2Cys6 DNA binding motif transcriptional activator FacB was cloned and is responsible for carbon source-, but not temperature-, dependent induction of acuD. The expression of acuD at 37°C is induced by AbaA, a key regulator of morphogenesis in P. marneffei, but deletion of abaA does not completely eliminate temperature-dependent induction, suggesting that acuD and the glyoxylate cycle are regulated by a complex network of factors in P. marneffei which may contribute to its pathogenicity. [source] Virulence, phenotype and genotype characteristics of endodontic Enterococcus spp.MOLECULAR ORAL MICROBIOLOGY, Issue 1 2005C. M. Sedgley Background/aims:, Enterococci have been implicated in persistent root canal infections but their role in the infection process remains unclear. This study investigated the virulence, phenotype and genotype of 33 endodontic enterococcal isolates. Methods:, Phenotypic tests were conducted for antibiotic resistance, clumping response to pheromone, and production of gelatinase, hemolysin and bacteriocin. Genotype analysis involved polymerase chain reaction amplification of virulence determinants encoding aggregation substances asa and asa373, cytolysin activator cylA, gelatinase gelE, gelatinase-negative phenotype ef1841/fsrC, adherence factors esp and ace, and endocarditis antigen efaA. Physical DNA characterization involved pulsed-field gel electrophoresis of genomic DNA, and plasmid analysis. Results:, Potential virulence traits expressed included production of gelatinase by Enterococcus faecalis (n = 23), and response to pheromones in E. faecalis culture filtrate (n = 16). Fourteen strains produced bacteriocin. Five strains were resistant to tetracycline and one to gentamicin, whereas all were susceptible to ampicillin, benzylpenicillin, chloramphenicol, erythromycin, fusidic acid, kanamycin, rifampin, streptomycin and vancomycin. Polymerase chain reaction products encoding efaA, ace, and asa were detected in all isolates; esp was detected in 20 isolates, cylA in six isolates, but asa373 was never detected. The gelatinase gene (gelE) was detected in all isolates of E. faecalis (n = 31) but not in Enterococcus faecium (n = 2); a 23.9 kb deletion sequence corresponding to the gelatinase-negative phenotype was detected in six of the eight E. faecalis isolates that did not produce gelatinase. Pulsed-field gel electrophoresis and plasmid analyses revealed genetic polymorphism with clonal types evident. Plasmid DNA was detected in 25 strains, with up to four plasmids per strain and a similar (5.1 kb) plasmid occurring in 16 isolates. Conclusions:, Phenotypic and genotypic evidence of potential virulence factors were identified in endodontic Enterococcus spp., specifically production of gelatinase and response to pheromones. [source] Protein kinase A subunits of the ascomycete pathogen Mycosphaerella graminicola regulate asexual fructification, filamentation, melanization and osmosensingMOLECULAR PLANT PATHOLOGY, Issue 6 2006RAHIM MEHRABI SUMMARY As in many fungi, asexual reproduction of Mycosphaerella graminicola in planta is a complex process that requires proper differentiation of the infectious hyphae in the substomatal cavities of foliar tissue before pycnidia with conidia can be formed. In this study, we have investigated the role of the cAMP signalling pathway in development and pathogenicity of this pathogen by disruption of the genes encoding the catalytic (designated MgTpk2) and regulatory subunit (designated MgBcy1) of protein kinase A. The MgTpk2 and MgBcy1 mutants showed altered phenotypes in vitro when grown under different growth conditions. On potato dextrose agar (PDA), MgBcy1 mutants showed altered osmosensitivity and reduced melanization, whereas the MgTpk2 mutants showed accelerated melanization when compared with the M. graminicola IPO323 wild-type strain and ectopic transformants. MgTpk2 mutants also secreted a dark-brown pigment into yeast glucose broth medium. In germination and microconidiation assays, both mutants showed a germination pattern similar to that of the controls on water agar, whereas on PDA filamentous growth of MgTpk2 mutants was impaired. Pathogenicity assays showed that the MgTpk2 and MgBcy1 mutants were less virulent as they caused only limited chlorotic and necrotic symptoms at the tips of the inoculated leaves. Further analyses of the infection process showed that MgTpk2 and MgBcy1 mutants were able to germinate, penetrate and colonize mesophyll tissue, but were unable to produce the asexual fructifications, which was particularly due to inappropriate differentiation during the late stage of this morphogenesis-related process. [source] Characterization of a developmentally regulated amino acid transporter (AAT1p) of the rust fungus Uromyces fabaeMOLECULAR PLANT PATHOLOGY, Issue 1 2002Christine Struck summary In the rust fungus Uromyces fabae, invasion of the host plant and haustorium formation are accompanied by the activation of many genes (PIGs =in planta induced genes). In addition to the previously described AAT2 (PIG2), AAT1 (PIG27) was found to encode a protein with a high similarity to fungal amino acid permeases. AAT1 transcripts are present in germinated hyphae and throughout the mycelium later in the infection process, but occur at the highest levels in haustoria. Expression of AAT1p in a histidine uptake-defective yeast mutant revealed energy-dependent transport of 14C-histidine, with a KM value of 25.8 µm. In addition, complementation analysis revealed AAT1 -dependent transport for lysine. Using Xenopus oocytes as expression system, AAT1p-dependent symport of protons with a broad spectrum of amino acids was observed, with the highest activities obtained with histidine and lysine. These results confirm that in rust fungi, the expression of amino acid transporters is developmentally regulated and occurs preferentially in the parasitic phase of development. [source] The distribution and expression of a biotrophy-related gene, CIH1, within the genus ColletotrichumMOLECULAR PLANT PATHOLOGY, Issue 4 2000Sarah E. Perfect During the biotrophic phase of the infection process of the hemibiotrophic anthracnose fungus Colletotrichum lindemuthianum, an intracellular hypha develops within epidermal cells of its host, Phaseolus vulgaris. This is followed by the formation of secondary hyphae during the necrotrophic phase. Previous work using a monoclonal antibody, UB25, has identified a glycoprotein that is specific to the interfacial matrix that forms between the wall of the intracellular hypha and the invaginated host plasma membrane. The gene encoding the protein identified by UB25 was cloned by immunoscreening and designated CIH1. The predicted amino acid sequence revealed a proline-rich glycoprotein, and biochemical evidence suggested that it formed a cross-linked structure at the biotrophic interface. Although CIH1 is a fungal gene, its product has several similarities to plant cell wall proteins. In this paper, we have surveyed the distribution and expression of CIH1 within the genus Colletotrichum, encompassing both necrotrophic and hemibiotrophic species. The results show that homologues of the CIH1 gene are present in all the Colletotrichum species tested. Northern blot studies of the time course of the infection process in planta have shown that CIH1 is expressed by both C. lindemuthianum in bean and C. trifolii in alfalfa during the biotrophic phase of fungal development. Immunofluorescence labelling of infected epidermal strips with UB25 revealed that the intracellular hyphae formed by C. destructivum as it infects alfalfa were specifically labelled in a similar way to those formed by C. lindemuthianum in bean. Northern and Western analysis showed that CIH1 was also expressed by C. lindemuthianum in vitro, though not constitutively. Overall, the evidence supports a role for CIH1 in biotrophy within the genus Colletotrichum. [source] Characterisation of the CipC-like protein AFUA_5G09330 of the opportunistic human pathogenic mould Aspergillus fumigatusMYCOSES, Issue 4 2010Bettina Bauer Summary,Aspergillus fumigatus is currently the major airborne fungal pathogen that menaces immunocompromised individuals. Germination of inhaled conidia is a hallmark of the early infection process, but little is known about the underlying mechanisms. The intention of our ongoing studies is the identification of A. fumigatus proteins that are differentially expressed during germination and may provide insights in the germination process. Using a proteomic approach, we identified AFUA_5G09330 as a major hyphal-specific protein. This result was confirmed using monoclonal antibodies generated in this study. AFUA_5G09330 belongs to a fungal-specific protein family. The eponymous CipC protein of A. nidulans has been shown to be induced by concanamycin A, and transcriptional data from Cryptococcus neoformans demonstrate a strong up-regulation of the expression of a homologous gene during infection. Our data provide evidence that AFUA_5G09330 is a monomeric, cytoplasmic protein. We found no evidence for an overexpression of AFUA_5G09330 induced by concanamycin A or other stress conditions. AFUA_5G09330 is exclusively found in the hyphal morphotype that enables an invasive growth of A. fumigatus during infection. Further studies are required to define the biological function of this hyphae-specific protein and its potential relevance for the pathogenicity of A. fumigatus. [source] Induction of systemic resistance in Arabidopsis thaliana in response to a culture filtrate from a plant growth-promoting fungus, Phoma sp.PLANT BIOLOGY, Issue 1 2009GS8- Abstract The plant growth-promoting fungus (PGPF), Phoma sp. GS8-3, isolated from a zoysia grass rhizosphere, is capable of protecting cucumber plants against virulent pathogens. This fungus was investigated in terms of the underlying mechanisms and ability to elicit systemic resistance in Arabidopsis thaliana. Root treatment of Arabidopsis plants with a culture filtrate (CF) from Phoma sp. GS8-3 elicited systemic resistance against the bacterial speck pathogen Pseudomonas syringae pv. tomato DC3000 (Pst), with restricted disease development and inhibited pathogen proliferation. Pathway-specific mutant plants, such as jar1 (jasmonic acid insensitive) and ein2 (ethylene insensitive), and transgenic NahG plants (impaired in salicylate signalling) were protected after application of the CF, demonstrating that these pathways are dispensable (at least individually) in CF-mediated resistance. Similarly, NPR1 interference in npr1 mutants had no effect on CF-induced resistance. Gene expression studies revealed that CF treatment stimulated the systemic expression of both the SA-inducible PR-1 and JA/ET-inducible PDF1.2 genes. However, pathogenic challenge to CF-treated plants was associated with potentiated expression of the PR-1 gene and down-regulated expression of the PDF1.2 gene. The observed down-regulation of the PDF1.2 gene in CF-treated plants indicates that there may be cross-talk between SA- and JA/ET-dependent signalling pathways during the pathogenic infection process. In conclusion, our data suggest that CF of Phoma sp. GS8-3 induces resistance in Arabidopsis in a manner where SA and JA/ET may play a role in defence signalling. [source] Effects of temperature and continuous and interrupted wetness on the infection of pear leaves by conidia of Venturia nashicolaPLANT PATHOLOGY, Issue 3 2005B.-H. Li Experiments were conducted to determine: (i) the effects of temperature and duration of continuous wet periods on the infection of pear seedlings by conidia of Venturia nashicola, the causal agent of pear scab; and (ii) the effects of the length and temperature of dry interrupting periods on the mortality of infecting conidia. Average number of scab lesions per leaf increased with increasing duration of wetness. Logistic models adequately described the change in the average number of scab lesions per leaf at 5, 10, 15, 20 and 25°C over the wetness duration. At 30°C, only a few lesions developed. Simple polynomial models satisfactorily described the relationship of the three logistic model parameters (maximum number of lesions, rate of appearance and the time to 50% of the maximum number of lesions) with temperature. The optimum temperature for infection was found to be approximately 20°C. The relationship between mortality and the length of a dry period interrupting an infection process can be satisfactorily described by an exponential model. The rate of mortality at 10, 16 and 22°C did not differ significantly, but was significantly less than that at 28°C. [source] Using the rate of respiration to monitor events in the infection of Escherichia coli cultures by bacteriophage T4BIOTECHNOLOGY PROGRESS, Issue 3 2010Dominic Sauvageau Abstract The growing interest in applications of bacteriophages creates a need for improvements in the production processes. Continuous monitoring of the phage production is an essential aspect of any control strategy and, at present, there is no completely satisfactory option. The approach presented here uses IR-spectrometry to continuously measure the rate of respiration (CO2 released) of Escherichia coli infected by phage T4 at various multiplicities of infection (MOI). Within the trends in these data, or in other aspects of the rate of respiration, it was possible to reliably and reproducibly identify five features that reflected specific events in the infection process. These included two events in the host cell apparent growth rate and events in the magnitude of the host cell density, in the measurement of OD600 or in the specific rate of respiration. All of these correlations were within 95% confidence showing that they are suitable for the monitoring and control of E. coli populations infected by phage T4. This method is reliable, cheap, and can be operated in-line and in real time. © 2009 American Institute of Chemical Engineers Biotechnol. Prog., 2010 [source] Microreview: Type IV secretion in the obligatory intracellular bacterium Anaplasma phagocytophilumCELLULAR MICROBIOLOGY, Issue 9 2010Yasuko Rikihisa Summary Anaplasma phagocytophilum is an obligatory intracellular bacterium that infects neutrophils, the primary host defence cells. Consequent effects of infection on host cells result in a potentially fatal systemic disease called human granulocytic anaplasmosis. Despite ongoing reductive genome evolution and deletion of most genes for intermediary metabolism and amino acid biosynthesis, Anaplasma has also experienced expansion of genes encoding several components of the type IV secretion (T4S) apparatus. Two A. phagocytophilum T4S effector molecules are currently known; Anaplasma translocated substrate 1 (Ats-1) and ankyrin repeat domain-containing protein A (AnkA) have C-terminal positively charged amino acid residues that are recognized by the T4S coupling protein, VirD4. AnkA and Ats-1 contain eukaryotic protein motifs and are uniquely evolved in the family Anaplasmataceae; Ats-1 contains a mitochondria-targeting signal. They are abundantly produced and secreted into the host cytoplasm, are not toxic to host cells, and manipulate host cell processes to aid in the infection process. At the cellular level, the two effectors have distinct subcellular localization and signalling in host cells. Thus in this obligatory intracellular pathogen, the T4S system has evolved as a host-subversive survival factor. [source] Infection of human mucosal tissue by Pseudomonas aeruginosa requires sequential and mutually dependent virulence factors and a novel pilus-associated adhesinCELLULAR MICROBIOLOGY, Issue 8 2010Ryan W. Heiniger Summary Tissue damage predisposes humans to life-threatening disseminating infection by the opportunistic pathogen Pseudomonas aeruginosa. Bacterial adherence to host tissue is a critical first step in this infection process. It is well established that P. aeruginosa attachment to host cells involves type IV pili (TFP), which are retractile surface fibres. The molecular details of attachment and the identity of the bacterial adhesin and host receptor remain controversial. Using a mucosal epithelium model system derived from primary human tissue, we show that the pilus-associated protein PilY1 is required for bacterial adherence. We establish that P. aeruginosa preferentially binds to exposed basolateral host cell surfaces, providing a mechanistic explanation for opportunistic infection of damaged tissue. Further, we demonstrate that invasion and fulminant infection of intact host tissue requires the coordinated and mutually dependent action of multiple bacterial factors, including pilus fibre retraction and the host cell intoxication system, termed type III secretion. Our findings offer new and important insights into the complex interactions between a pathogen and its human host and provide compelling evidence that PilY1 serves as the principal P. aeruginosa adhesin for human tissue and that it specifically recognizes a host receptor localized or enriched on basolateral epithelial cell surfaces. [source] Iron enhances endothelial cell activation in response to Cytomegalovirus or Chlamydia pneumoniae infectionEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2006A. E. R. Kartikasari Abstract Background, Chronic inflammation has been implemented in the pathogenesis of inflammatory diseases like atherosclerosis. Several pathogens like Chlamydia pneumoniae (Cp) and cytomegalovirus (CMV) result in inflammation and thereby are potentially artherogenic. Those infections could trigger endothelial activation, the starting point of the atherogenic inflammatory cascade. Considering the role of iron in a wide range of infection processes, the presence of iron may complicate infection-mediated endothelial activation. Materials and methods, Endothelial intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) expression were measured using flow cytometry, as an indication of endothelial activation. Cytotoxicity was monitored using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Immunostaining was applied to measure Cp and CMV infectivity to endothelial cells. Results, An increased number of infected endothelial cells in a monolayer population leads to a raised expression of adhesion molecules of the whole cell population, suggesting paracrine interactions. Iron additively up-regulated Cp-induced VCAM-1 expression, whereas synergistically potentiated Cp-induced ICAM-1 expression. Together with CMV, iron also enhanced ICAM-1 and VCAM-1 expression. These iron effects were observed without modulation of the initial infectivity of both microorganisms. Moreover, the effects of iron could be reversed by intracellular iron chelation or radical scavenging, conforming modulating effects of iron on endothelial activation after infections. Conclusions, Endothelial response towards chronic infections depends on intracellular iron levels. Iron status in populations positive for Cp or CMV infections should be considered as a potential determinant for the development of atherosclerosis. [source] Transmission dynamics of lymphatic filariasis: vector-specific density dependence in the development of Wuchereria bancrofti infective larvae in mosquitoesMEDICAL AND VETERINARY ENTOMOLOGY, Issue 3 2006L. C. SNOW Abstract The principles of meta-analysis developed in a previous study were extended to investigate the process of Wuchereria bancrofti (Cobbold) (Filarioidea: Onchocercidae) infection in mosquito (Diptera: Culicidae) hosts, focusing specifically on the functional forms and strength of density dependence in the development of ingested microfilariae (mf) to infective (third instar) larvae (L3). Mathematical models describing observed mf,L3 functional responses for each of the major three parasite-transmitting vector genera, Aedes, Culex and Anopheles mosquitoes, were fitted to paired mf,L3 data collated from all available studies in the published literature. Model parameters were estimated and compared by deriving and applying a data synthetic framework, based on applying a non-linear weighted regression model for fitting mathematical models to multistudy data. The results confirm previous findings of the existence of significant between-genera differences in the mf,L3 development relationship, particularly with regard to the occurrence of limitation in Culex mosquitoes and facilitation in Aedes and Anopheles mosquitoes. New and unexpected findings regarding L3 development from ingested mf were discovered as follows: (1) for Culex, overcompensation in L3 development at higher intensities of mf (or a peaked mf,L3 functional response) was detected; (2) for Aedes mosquitoes, facilitation (with an apparent asymptotic constraint on L3 development at high mf densities) was shown to be the major process governing L3 development, and (3) for Anopheles, a stronger facilitation type of response with no apparent saturation in L3 development appears to govern L3 output from ingested mf. These results yield major new insights regarding filarial vector infection dynamics and their potential impacts on parasite control, and demonstrate the efficacy of employing a data synthetic approach to reveal and estimate parasitic infection processes in host populations. [source] Rhesus monkey model for Leishmania major transmitted by Phlebotomus papatasi sandfly bitesMEDICAL AND VETERINARY ENTOMOLOGY, Issue 1 2001R. J. Probst Summary Leishmaniasis research needs a near-human model for investigations of natural infection processes, immunological responses and evaluation of treatments. Therefore, we developed a reproducible system using Leishmania major Yakimoff & Schokhor (Trypanosomatidae: Kinetoplastida), the cause of Old World zoonotic cutaneous leishmaniasis (ZCL), transmitted to rhesus monkeys Macaca mulatta (Zimmerman) (Primates: Cercopithecidae) by sandfly bites of experimentally infected Phlebotomus papatasi (Scopoli) (Diptera: Psychodidae). Eight monkeys of presumed Indian origin (Leishmania naïve) were exposed to bites of female sandflies that had been infected with L. major by membrane-feeding on human blood seeded with amastigotes isolated from hamster footpad lesions. Infection rates of membrane-fed sandflies averaged >,85% seven days after the infective feed, with uniformly high numbers of promastigotes in the stomodaeal valve region of the sandfly gut. Nodules and ulcerating dermal lesions developed on 7/8 monkeys 2,4 weeks post-bite and persisted for 3,7 months. Monkeys also developed satellite lesions beyond the area of sandfly bites on the head, but not on the chest. Three re-challenged monkeys developed lesions that healed faster than lesions from their primary challenges. After infection, monkeys developed delayed type hypersensitivity (DTH) responses to a panel of Leishmania skin test antigens (LSTA) and, when tested by ELISA and IFA, showed significant post-infection antibody titres which typically rose for ,170 days and then gradually receded during the next 100 days following the first challenge. After the second challenge, antibody titres spiked higher within ,50 days and receded more rapidly. In contrast, four rhesus macaques of Chinese origin developed no lesions following infected sandfly bites, although they raised antibodies and LSTA reactions, indicating subclinical infection. [source] A novel Phytophthora infestans haustorium-specific membrane protein is required for infection of potatoCELLULAR MICROBIOLOGY, Issue 11 2008Anna O. Avrova Summary Phytophthora infestans causes late-blight, a devastating and re-emerging disease of potato crops. During the early stages of infection, P. infestans differentiates infection-specific structures such as appressoria for host epidermal cell penetration, followed by infection vesicles, and haustoria to establish a biotrophic phase of interaction. Here we report the cloning, from a suppression subtractive hybridization library, of a P. infestans gene called Pihmp1 encoding a putative glycosylated protein with four closely spaced trans -membrane helices. Pihmp1 expression is upregulated in germinating cysts and in germinating cysts with appressoria, and significantly upregulated throughout infection of potato. Transient gene silencing of Pihmp1 led to loss of pathogenicity and indicated involvement of this gene in the penetration and early infection processes of P. infestans. P. infestans transformants expressing a Pihmp1::monomeric red fluorescent protein (mRFP) fusion demonstrated that Pihmp1 was translated in germinating sporangia, germinating cysts and appressoria, accumulated in the appressorium, and was located at the haustorial membrane during infection. Furthermore, we discovered that haustorial structures are formed over a 3 h period, maturing for up to 12 h, and that their formation is initiated only at sites on the surface of intercellular hyphae where Pihmp1::mRFP is localized. We propose that Pihmp1 is an integral membrane protein that provides physical stability to the plasma membrane of P. infestans infection structures. We have provided the first evidence that the surface of oomycete haustoria possess proteins specific to these biotrophic structures, and that formation of biotrophic structures (infection vesicles and haustoria) is essential to successful host colonization by P. infestans. [source] Characterization of the Biomechanical Properties of T4 Pili Expressed by Streptococcus pneumoniae,A Comparison between Helix-like and Open Coil-like PiliCHEMPHYSCHEM, Issue 9-10 2009Mickaël Castelain Dr. Abstract Adhesion strategies: Open coil-like T4 pili use different adhesion strategies in the presence of external forces (see figure) compared to the helix-like P pili. When exposed to significant forces, bacteria expressing helix-like pili remain attached by distributing the external force among a multitude of pili, whereas bacteria expressing open coil-like pili sustain large forces primarily by their multitude of binding adhesins. Bacterial adhesion organelles, known as fimbria or pili, are expressed by Gram-positive as well as Gram-negative bacteria families. These appendages play a key role in the first steps of the invasion and infection processes, and they therefore provide bacteria with pathogenic abilities. To improve the knowledge of pili-mediated bacterial adhesion to host cells and how these pili behave under the presence of an external force, we first characterize, using force measuring optical tweezers, open coil-like T4 pili expressed by Gram-positive Streptococcus pneumoniae with respect to their biomechanical properties. It is shown that their elongation behavior can be well described by the worm-like chain model and that they possess a large degree of flexibility. Their properties are then compared with those of helix-like pili expressed by Gram-negative uropathogenic Escherichia coli (UPEC), which have different pili architecture. The differences suggest that these two types of pili have distinctly dissimilar mechanisms to adhere and sustain external forces. Helix-like pili expressed by UPEC bacteria adhere to host cells by single adhesins located at the distal end of the pili while their helix-like structures act as shock absorbers to dampen the irregularly shear forces induced by urine flow and to increase the cooperativity of the pili ensemble, whereas open coil-like pili expressed by S. pneumoniae adhere to cells by a multitude of adhesins distributed along the pili. It is hypothesized that these two types of pili represent different strategies of adhering to host cells in the presence of external forces. When exposed to significant forces, bacteria expressing helix-like pili remain attached by distributing the external force among a multitude of pili, whereas bacteria expressing open coil-like pili sustain large forces primarily by their multitude of binding adhesins which presumably detach sequentially. [source] | ||||||||||||||||||||||||||||