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The genetics of non-host disease resistance in wheat to barley yellow rust

Rodrigues, Paula; Garrood, J.M.; Shen, Q.-H.; Smith, P.H.; Boyd, L.A.
Fonte: Springer-Verlag Publicador: Springer-Verlag
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
56.18%
Non-host resistance is investigated as a potential source of durable resistance. However, the genetics of non-host resistance between closely related plant species and their corresponding pathogens would indicate that in these interactions, non-host resistance primarily involves major genes that operate on a gene-for-gene principal similar to that seen in host resistance. Wheat is a non-host of the barley-attacking form of the fungus responsible for yellow rust, i.e. Puccinia striiformis f. sp. hordei. While P. striiformis f. sp. hordei is generally unable to infect wheat, a partial susceptibility was exhibited by the wheat variety Chinese 166. Consequently, in the cross Lemhi × Chinese 166 two major QTLs for resistance to P. striiformis f. sp. hordei were identified: one on chromosome 1D and a second on 2B. These two QTLs accounted for 43.5% and 33.2% of the phenotypic variance for resistance to barley yellow rust, respectively. In addition, two QTLs of smaller effect were also identified: one on chromosome 5A, contributing 5.1% of the variance and a second on chromosome 6A, contributing 10.9% to the phenotype. The QTL on 6A was derived from the susceptible variety, Chinese 166. In all cases the resistance towards P. striiformis f. sp. hordei was associated with a visual chlorosis/necrosis response typical of race specific host resistance.

Identification of non-host resistance genesin wheat to Puccinia striiformis f. sp. hordei

Rodrigues, Paula
Fonte: Universidade de Trás-os-Montes e Alto Douro Publicador: Universidade de Trás-os-Montes e Alto Douro
Tipo: Dissertação de Mestrado
ENG
Relevância na Pesquisa
66.13%
Yellow rust, caused by Puccinia striiformis West., is an important foliar disease of wheat and barley throughout the world, and the development of resistant cultivars is the most economical and environmentally friendly method of control. Breeding for resistance to yellow rust has, for decades, been based on the use of race-specific resistance genes, which have shown to be short-lived. Non-host resistance has been studied as a possible source of durable resistance. Two major genes, as well as an undetermined number of minor genes, for non-host resistance to the barley attacking form of yellow rust, P. striiformis f. sp. hordei, have been previously detected in the wheat cultivar ‘Lemhi’. The present study aimed at quantifying and mapping those genes using QTL (quantitative trait loci) mapping procedures. For that purpose, an F2 population of 114 individuals resulting from the cross of resistant ‘Lemhi’ with ‘Chinese 166’, a wheat cultivar susceptible to barley yellow rust, was used as the mapping population. QTL effects and significance were estimated by means of interval mapping and MQM mapping procedures. A map for the F2 population was constructed which included 116 DNA markers (14 SSRs and 102 AFLPs). Two major QTLs have been mapped to chromosome arms 1DS (Psh1) and 2BL (Psh2)...

Identification of non-host resistance genes in wheat to barley yellow rust

Rodrigues, Paula; Garrood, J.M.; Shen, Q.-H.; Smith, P.H.; Boyd, L.A.
Fonte: John Innes Centre Publicador: John Innes Centre
Tipo: Conferência ou Objeto de Conferência
ENG
Relevância na Pesquisa
66.13%
Yellow rust, caused by Puccinia striiformis West., is an important foliar disease of wheat and barley throughout the world, and the development of resistant cultivars is the most economical and environmentally friendly method of control. Breeding for resistance to yellow rust has, for decades, been based on the use of race-specific resistance genes, which have shown to be short-lived. Non-host resistance has been studied as a possible source of durable resistance. Two major genes, as well as an undetermined number of minor genes, for non-host resistance to the barley attacking form of yellow rust, P. striiformis f. sp. hordei, have been previously detected in the wheat cultivar ‘Lemhi’. The present study aimed at quantifying and mapping those genes using QTL (quantitative trait loci) mapping procedures. For that purpose, an F2 population of 114 individuals resulting from the cross of resistant ‘Lemhi’ with ‘Chinese 166’, a wheat cultivar susceptible to barley yellow rust, was used as the mapping population. QTL effects and significance were estimated by means of interval mapping and MQM mapping procedures. A map for the F2 population was constructed which included 116 DNA markers (14 SSRs and 102 AFLPs). Two major QTLs have been mapped to chromosome arms 1DS (Psh1) and 2BL (Psh2)...

Non-host resistance: is it really a durable source of resistance?

Rodrigues, Paula; Garrood, J.M.; Shen, Q.-H.; Smith, P.H.; Boyd, L.A.
Fonte: The British Society for Plant Pathology Publicador: The British Society for Plant Pathology
Tipo: Conferência ou Objeto de Conferência
ENG
Relevância na Pesquisa
66.19%
Yellow rust, caused by Puccinia striiformis West., is an important foliar disease of wheat and barley throughout the world, and the development of resistant cultivars is the most economical and environmentally friendly method of control. Breeding for resistance to yellow rust has, for decades, been based on the use of race-specific resistance genes, which have shown to be short-lived. Non-host resistance has been studied as a possible source of durable resistance. A non-host resistance associated with hypersensitivity has been detected in the wheat cultivar ‘Lemhi’ to the barley attacking form of yellow rust, P. striiformis f. sp. hordei. Two major genes, as well as an undetermined number of minor genes, have been identified as responsible for this resistance in ‘Lemhi’. The present study aimed at quantifying and mapping those genes using QTL (quantitative trait loci) mapping procedures. For that purpose, an F2 population of 114 individuals resulting from the cross of resistant ‘Lemhi’ with ‘Chinese 166’, a wheat cultivar susceptible to barley yellow rust, was used as the mapping population. QTL effects and significance were estimated by means of interval mapping and MQM mapping procedures. In all individuals showing resistance towards P. striiformis f.sp. hordei...

Field resistance of potato cultivars to foliar early blight and its relationship with foliage maturity and tuber skin types

Duarte,Henrique S. S.; Zambolim,Laércio; Rodrigues,Fabrício A.; Paul,Pierce A.; Pádua,Joaquim G.; Ribeiro Júnior,José I.; N. Júnior,Antonio F.; Rosado,André W. C.
Fonte: Sociedade Brasileira de Fitopatologia Publicador: Sociedade Brasileira de Fitopatologia
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/08/2014 EN
Relevância na Pesquisa
55.95%
Three field experiments were carried out to assess the level of resistance of several cultivars to early blight (EB) and to examine the association between host resistance and either foliage maturity or tuber skin types. A total of 26 cultivars were used in Exps. 1 and 2, and 24 in Exp. 3. Plants were inoculated with isolates of Alternaria grandis at 31 days after planting. EB severity was quantified in each plot every seven days. The approach to determine the resistance levels of potato cultivars was based on multivariate analysis techniques. The tested cultivars responded as either resistant, moderately resistant, moderately susceptible or susceptible to EB. Most of the cultivars were classified as susceptible or moderately susceptible to EB. Resistant cultivars were mid-season, mid-late or late maturity. None of the susceptible cultivars were later maturity (mid-late or late maturity). In most cases, susceptible cultivars were earlier maturity (early or mid-early maturity). Most resistant cultivars had rough, mid-rough or smooth skin. None of the susceptible cultivars had rough skin. In most cases, susceptible or moderately susceptible cultivars had smooth skin. Obtaining potato cultivars that are resistant to this destructive disease will help reduce production costs and the need for costly fungicides.

Interference between Host Resistance to Listeria monocytogenes Infection and Ovalbumin-Induced Allergic Responses in Mice

Mizuki, Daisuke; Miura, Tomisato; Sasaki, Sanae; Mizuki, Mayuko; Madarame, Hiroo; Nakane, Akio
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /03/2001 EN
Relevância na Pesquisa
55.89%
Listeria monocytogenes promotes the induction of the T-helper 1 (Th1) cell response, while ovalbumin (OVA) induces a Th2 cell response and allergic reactions, such as airway hyperreactivity and immunoglobulin E (IgE) production. When mice were immunized with OVA on day 7 after L. monocytogenes infection, eosinophilia in bronchoalveolar lavage and the production of total IgE, OVA-specific IgE, interleukin-4 (IL-4), and IL-5 in the circulation were markedly suppressed. Cytokine responses, including IL-4, IL-5, IL-10, IL-13, and gamma interferon, to OVA were decreased in the spleen cell cultures obtained from OVA-immunized mice that had been infected with L. monocytogenes. Conversely, when OVA-immunized mice were infected with L. monocytogenes, conversion from the nonlethal infection to the lethal infection occurred. Host resistance to L. monocytogenes infection in OVA-immunized mice was enhanced by the administration of anti–IL-10 monoclonal antibody. The present study indicates that striking interference is observed between Th1-inducing L. monocytogenes infection and Th2-driven OVA-induced airway hyperreactivity.

Effect of 6-Hydroxydopamine on Host Resistance against Listeria monocytogenes Infection

Miura, Tomisato; Kudo, Tsuyoshi; Matsuki, Akitomo; Sekikawa, Kenji; Tagawa, Yoh-Ichi; Iwakura, Yoichiro; Nakane, Akio
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /12/2001 EN
Relevância na Pesquisa
56.1%
Recent studies have shown that immunocompetent cells bear receptors of neuropeptides and neurotransmitters and that these ligands play roles in the immune response. In this study, the role of the sympathetic nervous system in host resistance against Listeria monocytogenes infection was investigated in mice pretreated with 6-hydroxydopamine (6-OHDA), which destroys sympathetic nerve termini. The norepinephrine contents of the plasma and spleens were significantly lower in 6-OHDA-treated mice than in vehicle-treated mice. The 50% lethal dose of L. monocytogenes was about 20 times higher for 6-OHDA-treated mice than for vehicle-treated mice. Chemical sympathectomy by 6-OHDA upregulated interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-α) production in enriched dendritic cell cultures and gamma interferon (IFN-γ) and TNF-α production in spleen cell cultures, whereas chemical sympathectomy had no apparent effect on phagocytic activities, listericidal activities, and nitric oxide production in peritoneal exudate cells and splenic macrophages. Augmentation of host resistance against L. monocytogenes infection by 6-OHDA was abrogated in IFN-γ−/− or TNF-α−/− mice, suggesting that upregulation of IFN-γ, IL-12, and TNF-α production may be involved in 6-OHDA-mediated augmentation of antilisterial resistance. Furthermore...

Comparison of Host Resistance to Primary and Secondary Listeria monocytogenes Infections in Mice by Intranasal and Intravenous Routes

Mizuki, Mayuko; Nakane, Akio; Sekikawa, Kenji; Tagawa, Yoh-ich; Iwakura, Yoichiro
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /09/2002 EN
Relevância na Pesquisa
56.07%
There have been no studies on the susceptibility and host immune responses to an intranasal infection with Listeria monocytogenes. In this study, we compared the susceptibilities and cytokine responses between intranasal and intravenous infections with L. monocytogenes in mice. Moreover, we compared efficiency of acquisition of host resistance to L. monocytogenes infection between intranasally and intravenously immunized mice because an intranasal immunization of vaccines is reportedly available for induction of adaptive immunity against various infectious pathogens. The susceptibility to an intranasal infection with L. monocytogenes was markedly lower than that to the intravenous infection. The bacterial growth in the lungs, spleens, and livers was substantially similar between intranasally and intravenously infected mice. Titers of endogenous gamma interferon (IFN-γ) and tumor necrosis factor-α (TNF-α) in the spleens, livers, and lungs were parallel to bacterial numbers in each organ of mice during intranasal infection and intravenous infection. IFN-γ-deficient mice and TNF-α-deficient mice were highly susceptible to intranasal infection as well as intravenous infection. Susceptibilities to intranasal and intravenous L. monocytogenes infection were the same in these cytokine-deficient mice. These results suggest that both IFN-γ and TNF-α play critical roles in host resistance to intranasal L. monocytogenes infection as well as the intravenous infection. Acquisition of host resistance to intravenous and intranasal L. monocytogenes infection was induced in intranasally immunized mice as well as intravenously immunized mice...

Effects of cannabinoids on host resistance to Listeria monocytogenes and herpes simplex virus.

Morahan, P S; Klykken, P C; Smith, S H; Harris, L S; Munson, A E
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /03/1979 EN
Relevância na Pesquisa
46.12%
Previous investigations from our laboratories have demonstrated that cannabinoids possess immunosuppressive properties. The present studies were designed to determine whether these agents decrease host resistance to infections with Listeria monocytogenes and herpes simplex virus type 2. Host resistance was measured by changes in the 50% lethal dose of the pathogen in cannabinoid-treated and control mice. The effect of cannabinoids on resistance to L. monocytogens was dose dependent. Delta-9-tetrhydrocannabinol at doses of 38, 75, and 150 mg/kg suppressed resistance to infection by 10-, 17-, and 657-fold, respectively. Marijuana extract was less active but significantly reduced resistance to L. moncytogenes at all tested doses. Resistance to systemic herpes simplex virus type 2 infection was decreased 96-fold by delta-9-tetrahydrocannabinol, although marijuana extract was inactive. The doses and regimen of treatment with cannabinoids that produced significant decreases in host resistance were similar to those which caused suppression of delayed-type hypersensitivity to sheep erythrocytes. The possible mechanisms and public health aspects of the decreased host resistance produced by marijuana extract and its cannabinoids are discussed.

Balance of Irgm protein activities determines IFN-γ-induced host defense

Henry, Stanley C.; Daniell, Xiaoju G.; Burroughs, Ashley R.; Indaram, Maanasa; Howell, David N.; Coers, Jörn; Starnbach, Michael N.; Hunn, Julia P.; Howard, Jonathan C.; Feng, Carl G.; Sher, Alan; Taylor, Gregory A.
Fonte: The Society for Leukocyte Biology Publicador: The Society for Leukocyte Biology
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.11%
The immunity-related GTPases (IRG), also known as p47 GTPases, are a family of proteins that are tightly regulated by IFNs at the transcriptional level and serve as key mediators of IFN-regulated resistance to intracellular bacteria and protozoa. Among the IRG proteins, loss of Irgm1 has the most profound impact on IFN-γ-induced host resistance at the physiological level. Surprisingly, the losses of host resistance seen in the absence of Irgm1 are sometimes more striking than those seen in the absence of IFN-γ. In the current work, we address the underlying mechanism. We find that in several contexts, another protein in the IRG family, Irgm3, functions to counter the effects of Irgm1. By creating mice that lack Irgm1 and Irgm3, we show that several phenotypes important to host resistance that are caused by Irgm1 deficiency are reversed by coincident Irgm3 deficiency; these include resistance to Salmonella typhimurium in vivo, the ability to affect IFN-γ-induced Salmonella killing in isolated macrophages, and the ability to regulate macrophage adhesion and motility in vitro. Other phenotypes that are caused by Irgm1 deficiency, including susceptibility to Toxoplasma gondii and the regulation of GKS IRG protein expression and localization...

Identification and utilization of a sow thistle powdery mildew as a poorly adapted pathogen to dissect post-invasion non-host resistance mechanisms in Arabidopsis

Wen, Yingqiang; Wang, Wenming; Feng, Jiayue; Luo, Ming-Cheng; Tsuda, Kenichi; Katagiri, Fumiaki; Bauchan, Gary; Xiao, Shunyuan
Fonte: Oxford University Press Publicador: Oxford University Press
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.1%
To better dissect non-host resistance against haustorium-forming powdery mildew pathogens, a sow thistle powdery mildew isolate designated Golovinomyces cichoracearum UMSG1 that has largely overcome penetration resistance but is invariably stopped by post-invasion non-host resistance of Arabidopsis thaliana was identified. The post-invasion non-host resistance is mainly manifested as the formation of a callosic encasement of the haustorial complex (EHC) and hypersensitive response (HR), which appears to be controlled by both salicylic acid (SA)-dependent and SA-independent defence pathways, as supported by the susceptibility of the pad4/sid2 double mutant to the pathogen. While the broad-spectrum resistance protein RPW8.2 enhances post-penetration resistance against G. cichoracearum UCSC1, a well-adapted powdery mildew pathogen, RPW8.2, is dispensable for post-penetration resistance against G. cichoracearum UMSG1, and its specific targeting to the extrahaustorial membrane is physically blocked by the EHC, resulting in HR cell death. Taken together, the present work suggests an evolutionary scenario for the Arabidopsis–powdery mildew interaction: EHC formation is a conserved subcellular defence evolved in plants against haustorial invasion; well-adapted powdery mildew has evolved the ability to suppress EHC formation for parasitic growth and reproduction; RPW8.2 has evolved to enhance EHC formation...

Altering Host Resistance to Infections through Microbial Transplantation

Willing, Benjamin P.; Vacharaksa, Anjalee; Croxen, Matthew; Thanachayanont, Teerawat; Finlay, B. Brett
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 28/10/2011 EN
Relevância na Pesquisa
46.1%
Host resistance to bacterial infections is thought to be dictated by host genetic factors. Infections by the natural murine enteric pathogen Citrobacter rodentium (used as a model of human enteropathogenic and enterohaemorrhagic E. coli infections) vary between mice strains, from mild self-resolving colonization in NIH Swiss mice to lethality in C3H/HeJ mice. However, no clear genetic component had been shown to be responsible for the differences observed with C. rodentium infections. Because the intestinal microbiota is important in regulating resistance to infection, and microbial composition is dependent on host genotype, it was tested whether variations in microbial composition between mouse strains contributed to differences in “host” susceptibility by transferring the microbiota of resistant mice to lethally susceptible mice prior to infection. Successful transfer of the microbiota from resistant to susceptible mice resulted in delayed pathogen colonization and mortality. Delayed mortality was associated with increased IL-22 mediated innate defense including antimicrobial peptides Reg3γ and Reg3β, and immunono-neutralization of IL-22 abrogated the beneficial effect of microbiota transfer. Conversely, depletion of the native microbiota in resistant mice by antibiotics and transfer of the susceptible mouse microbiota resulted in reduced innate defenses and greater pathology upon infection. This work demonstrates the importance of the microbiota and how it regulates mucosal immunity...

Heme Catabolism by Heme Oxygenase-1 Confers Host Resistance to Mycobacterium Infection

Silva-Gomes, Sandro; Appelberg, Rui; Larsen, Rasmus; Soares, Miguel Parreira; Gomes, Maria Salomé
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /07/2013 EN
Relevância na Pesquisa
55.93%
Heme oxygenases (HO) catalyze the rate-limiting step of heme degradation. The cytoprotective action of the inducible HO-1 isoform, encoded by the Hmox1 gene, is required for host protection against systemic infections. Here we report that upregulation of HO-1 expression in macrophages (Mϕ) is strictly required for protection against mycobacterial infection in mice. HO-1-deficient (Hmox1−/−) mice are more susceptible to intravenous Mycobacterium avium infection, failing to mount a protective granulomatous response and developing higher pathogen loads, than infected wild-type (Hmox1+/+) controls. Furthermore, Hmox1−/− mice also develop higher pathogen loads and ultimately succumb when challenged with a low-dose aerosol infection with Mycobacterium tuberculosis. The protective effect of HO-1 acts independently of adaptive immunity, as revealed in M. avium-infected Hmox1−/− versus Hmox1+/+ SCID mice lacking mature B and T cells. In the absence of HO-1, heme accumulation acts as a cytotoxic pro-oxidant in infected Mϕ, an effect mimicked by exogenous heme administration to M. avium-infected wild-type Mϕ in vitro or to mice in vivo. In conclusion, HO-1 prevents the cytotoxic effect of heme in Mϕ, contributing critically to host resistance to Mycobacterium infection.

Host resistance influences patterns of experimental viral adaptation and virulence evolution

Kubinak, Jason L; Potts, Wayne K
Fonte: Landes Bioscience Publicador: Landes Bioscience
Tipo: Artigo de Revista Científica
EN
Relevância na Pesquisa
46.13%
Infectious diseases are major threats to all living systems, so understanding the forces of selection that limit the evolution of more virulent pathogens is of fundamental importance; this includes the practical application of identifying possible mitigation strategies for at-risk host populations. The evolution of more virulent pathogens has been classically understood to be limited by the tradeoff between within-host growth rate and transmissibility. Importantly, heterogeneity among hosts can influence both of these factors. However, despite our substantial understanding of how the immune system operates to control pathogen replication during infection, we have only a limited appreciation of how variability in intrinsic (i.e., genetically determined) levels of host resistance influences patterns of pathogen adaptation and virulence evolution. Here, we describe results from experimental evolution studies using a model host–pathogen (virus–mammal) system; we demonstrate that variability in intrinsic levels of resistance among host genotypes can have significant effects on patterns of pathogen adaptation and virulence evolution during serial passage. Both the magnitude of adaptive response as well as the degree of pathogen specialization was positively correlated with host resistance...

Characterization of Arabidopsis Transcriptional Responses to Different Aphid Species Reveals Genes that Contribute to Host Susceptibility and Non-host Resistance

Jaouannet, Maëlle; Morris, Jenny A.; Hedley, Peter E.; Bos, Jorunn I. B.
Fonte: Public Library of Science Publicador: Public Library of Science
Tipo: Artigo de Revista Científica
Publicado em 20/05/2015 EN
Relevância na Pesquisa
46.1%
Aphids are economically important pests that display exceptional variation in host range. The determinants of diverse aphid host ranges are not well understood, but it is likely that molecular interactions are involved. With significant progress being made towards understanding host responses upon aphid attack, the mechanisms underlying non-host resistance remain to be elucidated. Here, we investigated and compared Arabidopsis thaliana host and non-host responses to aphids at the transcriptional level using three different aphid species, Myzus persicae, Myzus cerasi and Rhopalosiphum pisum. Gene expression analyses revealed a high level of overlap in the overall gene expression changes during the host and non-host interactions with regards to the sets of genes differentially expressed and the direction of expression changes. Despite this overlap in transcriptional responses across interactions, there was a stronger repression of genes involved in metabolism and oxidative responses specifically during the host interaction with M. persicae. In addition, we identified a set of genes with opposite gene expression patterns during the host versus non-host interactions. Aphid performance assays on Arabidopsis mutants that were selected based on our transcriptome analyses identified novel genes contributing to host susceptibility...

Effectors of biotrophic fungi and oomycetes: pathogenicity factors and triggers of host resistance

Dodds, Peter N; Rafiqi, Maryam; Gan, Pamela H P; Hardham, Adrienne R; Jones, David A; Ellis, Jeffrey G
Fonte: Wiley Publicador: Wiley
Tipo: Artigo de Revista Científica Formato: 8 pages
Relevância na Pesquisa
56.04%
Many biotrophic fungal and oomycete pathogens share a common infection process involving the formation of haustoria, which penetrate host cell walls and form a close association with plant membranes. Recent studies have identified a class of patho- genicity effector proteins from these pathogens that is transferred into host cells from haustoria during infection. This insight stemmed from the identification of avirulence (Avr) proteins from these pathogens that are recognized by intracellular host resistance (R) proteins. Oomycete effectors contain a conserved translocation motif that directs their uptake into host cells independently of the pathogen, and is shared with the human malaria pathogen. Genome sequence information indicates that oomycetes may express several hundred such host-translocated effectors. Elucidating the transport mechanism of fungal and oomycete effectors and their roles in disease offers new opportunities to understand how these pathogens are able to manipulate host cells to establish a parasitic relationship and to develop new disease-control measures.; Work in the authors’ laboratories is supported by Australian Research Council grant DP0771374 and the Grains Research and Development Corporation.

Production of reactive oxygen species during non-specific elicitation, non-host resistance and field resistance expression in cultured tobacco cells

Able, A.; Sutherland, M.; Guest, D.
Fonte: C S I R O Publishing Publicador: C S I R O Publishing
Tipo: Artigo de Revista Científica
Publicado em //2003 EN
Relevância na Pesquisa
56%
We examined production of reactive oxygen species (ROS) and induction of cell death in tissue-cultured tobacco cells undergoing different disease resistance responses. A superoxide-dependent hypersensitive response occurs during both the race-specific resistance response of tobacco cells challenged with incompatible zoospores of Phytophthora nicotianae and during non-specific elicitation of tobacco cells challenged with Phytophthora glucan elicitors extracted from the fungal cell wall. Inhibition studies are consistent with dependence upon endogenous Ca2+ levels, and with involvement of NAD(P)H oxidase and peroxidases in production of ROS during both specific and non-specific elicitation. The patterns of resistance expression during non-host resistance or field resistance responses appear to be similar to race-specific resistance expression with regard to the timing and order of events. However, the intensity of the response is very much reduced. In contrast, during non-specific elicitation, these temporal patterns are significantly altered. The differences in timing, intensity and extent of responses during different modes of disease resistance expression indicate that stimulation of cultured plant cells with non-specific soluble fractions in order to model in planta events during plant / Oomycete and...

Cassytha pubescens: germination biology and interactions with native and introduced hosts.

Tsang, Hong Tai (Steven)
Fonte: Universidade de Adelaide Publicador: Universidade de Adelaide
Tipo: Tese de Doutorado
Publicado em //2010
Relevância na Pesquisa
46.13%
The native hemiparasitic vine Cassytha pubescens infects and often kills the invasive weeds Cytisus scoparius and Ulex europaeus in the Mount Lofty Ranges, South Australia. This leads to the consideration of whether this parasite is a suitable biological control agent for these weeds. The aims of this study were to investigate germination characteristics of the parasite, the direct effects of the parasite on both invasive and native hosts, and the indirect effects of the parasite on interactions between native and invasive hosts. Seed dormancy and germination of C. pubescens were examined. Imbibition tests revealed that the seeds are enclosed in a water impermeable seed coat, which produces physical dormancy. Germination experiments showed that heat and scarification broke the physical dormancy, but the germination rate of heated seeds was over three times higher than that of scarified seeds. Thus this parasite may have evolved to share similar fire-related germination cues as some of its native hosts. The direct impact of C. pubescens on growth of Acacia myrtifolia (a native legume) and Cytisus scoparius (an invasive legume) was investigated in a pot experiment. None of the parasites on infected A. myrtifolia survived, so none of the A. myrtifolia was successfully infected with the parasite. In contrast...

Heme catabolism by heme oxygenase-1 confers host resistance to Mycobacterium infection

Silva-Gomes, Sandro; Appelberg, Rui; Larsen, Rasmus; Soares, Miguel Parreira; Gomes, Maria Salomé
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /07/2013 ENG
Relevância na Pesquisa
55.95%
Heme oxygenases (HO) catalyze the rate-limiting step of heme degradation. The cytoprotective action of the inducible HO-1 isoform, encoded by the Hmox1 gene, is required for host protection against systemic infections. Here we report that upregulation of HO-1 expression in macrophages (M) is strictly required for protection against mycobacterial infection in mice. HO-1-deficient (Hmox1(-/-)) mice are more susceptible to intravenous Mycobacterium avium infection, failing to mount a protective granulomatous response and developing higher pathogen loads, than infected wild-type (Hmox1(+/+)) controls. Furthermore, Hmox1(-/-) mice also develop higher pathogen loads and ultimately succumb when challenged with a low-dose aerosol infection with Mycobacterium tuberculosis. The protective effect of HO-1 acts independently of adaptive immunity, as revealed in M. avium-infected Hmox1(-/-) versus Hmox1(+/+) SCID mice lacking mature B and T cells. In the absence of HO-1, heme accumulation acts as a cytotoxic pro-oxidant in infected M, an effect mimicked by exogenous heme administration to M. avium-infected wild-type M in vitro or to mice in vivo. In conclusion, HO-1 prevents the cytotoxic effect of heme in M, contributing critically to host resistance to Mycobacterium infection.; European Community 6th Framework grant: (LSH-2005-1.2.5-1)...

Toxoplasma gondii Rhoptry 16 Kinase Promotes Host Resistance to Oral Infection and Intestinal Inflammation Only in the Context of the Dense Granule Protein GRA15

Jensen, Kirk D. C.; Hu, Kenneth; Whitmarsh, Ryan J.; Hassan, Musa A.; Julien, Lindsay; Lu, Diana; Chen, Lieping; Hunter, Christopher A.; Saeij, Jeroen P. J.
Fonte: American Society for Microbiology Publicador: American Society for Microbiology
Tipo: Artigo de Revista Científica
Publicado em /06/2013 EN
Relevância na Pesquisa
56.08%
Toxoplasma gondii transmission between intermediate hosts is dependent on the ingestion of walled cysts formed during the chronic phase of infection. Immediately following consumption, the parasite must ensure survival of the host by preventing adverse inflammatory responses and/or by limiting its own replication. Since the Toxoplasma secreted effectors rhoptry 16 kinase (ROP16) and dense granule 15 (GRA15) activate the JAK-STAT3/6 and NF-κB signaling pathways, respectively, we explored whether a particular combination of these effectors impacted intestinal inflammation and parasite survival in vivo. Here we report that expression of the STAT-activating version of ROP16 in the type II strain (strain II+ROP16I) promotes host resistance to oral infection only in the context of endogenous GRA15 expression. Protection was characterized by a lower intestinal parasite burden and dampened inflammation. Host resistance to the II+ROP16I strain occurred independently of STAT6 and the T cell coinhibitory receptors B7-DC and B7-H1, two receptors that are upregulated by ROP16. In addition, coexpression of ROP16 and GRA15 enhanced parasite susceptibility within tumor necrosis factor alpha/gamma interferon-stimulated macrophages in a STAT3/6-independent manner. Transcriptional profiling of infected STAT3- and STAT6-deficient macrophages and parasitized Peyer's patches from mice orally challenged with strain II+ROP16I suggested that ROP16 activated STAT5 to modulate host gene expression. Consistent with this supposition...