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1
Waalwijk, Cees, and Jacq R. A. De Koning. "Towards Isolation of Avirulence Factors in Fusarium Oxysporum from Carnation." Cereal Research Communications 25, no. 3 (September 1997): 841–43. http://dx.doi.org/10.1007/bf03543869.
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Janzac, Bérenger, Josselin Montarry, Alain Palloix, Olivier Navaud, and Benoît Moury. "A Point Mutation in the Polymerase of Potato virus Y Confers Virulence Toward the Pvr4 Resistance of Pepper and a High Competitiveness Cost in Susceptible Cultivar." Molecular Plant-Microbe Interactions® 23, no. 6 (June 2010): 823–30. http://dx.doi.org/10.1094/mpmi-23-6-0823.
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To understand why the Pvr4 resistance of pepper against Potyvirus spp. remained durable in field conditions while virulent Potato virus Y (PVY) variants could be selected in the laboratory, we studied the molecular mechanisms which generated these variants and the consequences on viral fitness. Using a reverse genetics approach with an infectious cDNA clone of PVY, we found that the region coding for the NIb protein (RNA-dependent RNA polymerase) of PVY was the avirulence factor corresponding to Pvr4 and that a single nonsynonymous nucleotide substitution in that region, an adenosine to guanosine substitution at position 8,424 of the PVY genome (A8424G), was sufficient for virulence. This substitution imposed a high competitiveness cost to the virus against an avirulent PVY variant in plants devoid of Pvr4. In addition, during serial passages in susceptible pepper plants, the only observed possibility of the virulent mutant to increase its fitness was through the G8424A reversion, strengthening the high durability potential of the Pvr4 resistance. This is in accordance with the fact that the NIb protein is one of the most constrained proteins expressed by the PVY genome and, more generally, by Potyvirus spp., and with a previously developed model predicting the durability of virus resistances as a function of the evolutionary constraint applied on corresponding avirulence factors.
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Zhu, Weiguang, Bing Yang, Jaishree M. Chittoor, Lowell B. Johnson, and Frank F. White. "AvrXa10 Contains an Acidic Transcriptional Activation Domain in the Functionally Conserved C Terminus." Molecular Plant-Microbe Interactions® 11, no. 8 (August 1998): 824–32. http://dx.doi.org/10.1094/mpmi.1998.11.8.824.
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The avrXa10 gene of Xanthomonas oryzae pv. oryzae, the causal agent of bacterial blight of rice, is a member of the avrBs3 avirulence gene family and directs the elicitation of resistance in a gene-for-gene manner on rice lines carrying the resistance gene Xa10. The carboxyl (C) terminus of AvrXa10 has a previously undescribed domain that is structurally similar to the acidic activation domain of many eukaryotic transcription factors in addition to three nuclear localization signal (NLS) sequences. Removal of the C-terminal 38 codons containing the putative activation domain, but retaining the NLS sequences, was concomitant with the loss of avirulence activity. The C-terminal coding regions of avrBs3 and avrXa7 can be replaced by the corresponding region of avrXa10, and the genes retained specificity for the resistance genes Bs3 in pepper and Xa7 in rice, respectively. The avrBs3 and avrXa7 avirulence activities of the hybrid genes were also lost upon removal of the terminal 38 codons. When fused to the coding sequence of the Gal4 DNA binding domain, AvrXa10 activated transcription in yeast and Arabidopsis thaliana. Removal of the carboxyl region severely reduced transcriptional activation. AvrXa10 would have to be localized to the host cell nucleus to function autonomously in transcriptional activation. Consistent with this requirement, mutations in all three NLS sequences of avrXa10 caused a loss in avirulence activity. The findings demonstrate the requirement of the C terminus for AvrXa10 function and the potential for the members of this family of avirulence gene products to enter the host nucleus and alter host transcription.
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Huang, Changjun. "From Player to Pawn: Viral Avirulence Factors Involved in Plant Immunity." Viruses 13, no. 4 (April 16, 2021): 688. http://dx.doi.org/10.3390/v13040688.
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In the plant immune system, according to the ‘gene-for-gene’ model, a resistance (R) gene product in the plant specifically surveils a corresponding effector protein functioning as an avirulence (Avr) gene product. This system differs from other plant–pathogen interaction systems, in which plant R genes recognize a single type of gene or gene family because almost all virus genes with distinct structures and functions can also interact with R genes as Avr determinants. Thus, research conducted on viral Avr-R systems can provide a novel understanding of Avr and R gene product interactions and identify mechanisms that enable rapid co-evolution of plants and phytopathogens. In this review, we intend to provide a brief overview of virus-encoded proteins and their roles in triggering plant resistance, and we also summarize current progress in understanding plant resistance against virus Avr genes. Moreover, we present applications of Avr gene-mediated phenotyping in R gene identification and screening of segregating populations during breeding processes.
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Huertas-González, M. D., M. C. Ruiz-Roldán, A. Di Pietro, and M. I. G. Roncero. "Cross protection provides evidence for race-specific avirulence factors inFusarium oxysporum." Physiological and Molecular Plant Pathology 54, no. 3-4 (March 1999): 63–72. http://dx.doi.org/10.1006/pmpp.1998.0185.
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Amezrou, Reda, Colette Audéon, Jérôme Compain, Sandrine Gélisse, Aurélie Ducasse, Cyrille Saintenac, Nicolas Lapalu, et al. "A secreted protease-like protein in Zymoseptoria tritici is responsible for avirulence on Stb9 resistance gene in wheat." PLOS Pathogens 19, no. 5 (May 12, 2023): e1011376. http://dx.doi.org/10.1371/journal.ppat.1011376.
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Zymoseptoria tritici is the fungal pathogen responsible for Septoria tritici blotch on wheat. Disease outcome in this pathosystem is partly determined by isolate-specific resistance, where wheat resistance genes recognize specific fungal factors triggering an immune response. Despite the large number of known wheat resistance genes, fungal molecular determinants involved in such cultivar-specific resistance remain largely unknown. We identified the avirulence factor AvrStb9 using association mapping and functional validation approaches. Pathotyping AvrStb9 transgenic strains on Stb9 cultivars, near isogenic lines and wheat mapping populations, showed that AvrStb9 interacts with Stb9 resistance gene, triggering an immune response. AvrStb9 encodes an unusually large avirulence gene with a predicted secretion signal and a protease domain. It belongs to a S41 protease family conserved across different filamentous fungi in the Ascomycota class and may constitute a core effector. AvrStb9 is also conserved among a global Z. tritici population and carries multiple amino acid substitutions caused by strong positive diversifying selection. These results demonstrate the contribution of an ‘atypical’ conserved effector protein to fungal avirulence and the role of sequence diversification in the escape of host recognition, adding to our understanding of host-pathogen interactions and the evolutionary processes underlying pathogen adaptation.
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Valent, B., L. Farrall, and F. G. Chumley. "Magnaporthe grisea genes for pathogenicity and virulence identified through a series of backcrosses." Genetics 127, no. 1 (January 1, 1991): 87–101. http://dx.doi.org/10.1093/genetics/127.1.87.
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Abstract We have identified genes for pathogenicity toward rice (Oryza sativa) and genes for virulence toward specific rice cultivars in the plant pathogenic fungus Magnaporthe grisea. A genetic cross was conducted between the weeping lovegrass (Eragrostis curvula) pathogen 4091-5-8, a highly fertile, hermaphroditic laboratory strain, and the rice pathogen O-135, a poorly fertile, female-sterile field isolate that infects weeping lovegrass as well as rice. A six-generation backcrossing scheme was then undertaken with the rice pathogen as the recurrent parent. One goal of these crosses was to generate rice pathogenic progeny with the high fertility characteristic of strain 4091-5-8, which would permit rigorous genetic analysis of rice pathogens. Therefore, progeny strains to be used as parents for backcross generations were chosen only on the basis of fertility. The ratios of pathogenic to nonpathogenic (and virulent to avirulent) progeny through the backcross generations suggested that the starting parent strains differ in two types of genes that control the ability to infect rice. First, they differ by polygenic factors that determine the extent of lesion development achieved by those progeny that infect rice. These genes do not appear to play a role in infection of weeping lovegrass because both parents and all progeny infect weeping lovegrass. Second, the parents differ by simple Mendelian determinants, "avirulence genes," that govern virulence toward specific rice cultivars in all-or-none fashion. Several crosses confirm the segregation of three unlinked avirulence genes, Avr 1-CO39, Avr 1-M201 and Avr1-YAMO, alleles of which determine avirulence on rice cultivars CO39, M201, and Yashiro-mochi, respectively. Interestingly, avirulence alleles of Avr1-CO39, Avr1-M201 and Avr1-YAMO were inherited from the parent strain 4091-5-8, which is a nonpathogen of rice. Middle repetitive DNA sequences ("MGR sequences"), present in approximately 40-50 copies in the genome of the rice pathogen parent, and in very low copy number in the genome of the nonpathogen of rice, were used as physical markers to monitor restoration of the rice pathogen genetic background during introgression of fertility. The introgression of highest levels of fertility into the most successful rice pathogen progeny was incomplete by the sixth generation, perhaps a consequence of genetic linkage between genes for fertility and genes for rice pathogenicity. One chromosomal DNA segment with MGR sequence homology appeared to be linked to the gene Avr1-CO39. Finally, many of the crosses described in this paper exhibited a characteristic common to many crosses involving M. grisea rice pathogen field isolates.(ABSTRACT TRUNCATED AT 400 WORDS)
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Webb, Craig A., and John P. Fellers. "Cereal rust fungi genomics and the pursuit of virulence and avirulence factors." FEMS Microbiology Letters 264, no. 1 (November 2006): 1–7. http://dx.doi.org/10.1111/j.1574-6968.2006.00400.x.
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Beams, Alexander B., Rebecca Bateman, and Frederick R. Adler. "Will SARS-CoV-2 Become Just Another Seasonal Coronavirus?" Viruses 13, no. 5 (May 7, 2021): 854. http://dx.doi.org/10.3390/v13050854.
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The future prevalence and virulence of SARS-CoV-2 is uncertain. Some emerging pathogens become avirulent as populations approach herd immunity. Although not all viruses follow this path, the fact that the seasonal coronaviruses are benign gives some hope. We develop a general mathematical model to predict when the interplay among three factors, correlation of severity in consecutive infections, population heterogeneity in susceptibility due to age, and reduced severity due to partial immunity, will promote avirulence as SARS-CoV-2 becomes endemic. Each of these components has the potential to limit severe, high-shedding cases over time under the right circumstances, but in combination they can rapidly reduce the frequency of more severe and infectious manifestation of disease over a wide range of conditions. As more reinfections are captured in data over the next several years, these models will help to test if COVID-19 severity is beginning to attenuate in the ways our model predicts, and to predict the disease.
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Bonshtien, Arale, Atar Lev, Avi Gibly, Paul Debbie, Adi Avni, and Guido Sessa. "Molecular Properties of the Xanthomonas AvrRxv Effector and Global Transcriptional Changes Determined by Its Expression in Resistant Tomato Plants." Molecular Plant-Microbe Interactions® 18, no. 4 (April 2005): 300–310. http://dx.doi.org/10.1094/mpmi-18-0300.
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The Xanthomonas campestris pv. vesicatoria avirulence gene avrRxv specifies resistance on the tomato line Hawaii 7998 by interacting with three nondominant plant resistance genes. AvrRxv molecular properties that impinge on its avirulence activity were characterized and transcriptional changes caused by AvrRxv expression in resistant tomato plants were extensively examined. AvrRxv localized predominantly to the cytoplasm and possibly in association with plasma and nuclear membranes in both resistant and susceptible tomato plants. The AvrRxv cysteine protease catalytic core was found to be essential for host recognition, because introduction of mutations in this domain affected the ability of AvrRxv to elicit a hypersensitive response and the inhibition of bacterial growth in resistant plants. In addition, expression profiles were analyzed for approximately 8,600 tomato genes in resistant plants challenged with X. campestris pv. vesicatoria strains expressing wild-type AvrRxv or a catalytic core AvrRxv mutant. In all, 420 genes were identified as differentially modulated by the expression of a functional AvrRxv, including over 15 functional classes of proteins and a large number of transcription factors and signaling components. Findings of this study allow the development of new hypotheses about the molecular basis of recognition between AvrRxv and the corresponding resistance proteins, and set the stage for the dissection of signaling and cellular responses triggered in tomato plants by this avirulence factor.
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Mhiri, Corinne, Pierre J. G. M. De Wit, and Marie-Angèle Grandbastien. "Activation of the Promoter of the Tnt1 Retrotransposon in Tomato After Inoculation with the Fungal Pathogen Cladosporium fulvum." Molecular Plant-Microbe Interactions® 12, no. 7 (July 1999): 592–603. http://dx.doi.org/10.1094/mpmi.1999.12.7.592.
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The copia-like Tnt1 element of tobacco is one of the few active plant retrotransposons and is transcriptionally activated, in tobacco and in heterologous species, by biotic and abiotic stress factors. In order to establish more precisely the link between Tnt1 activation and plant defense responses, the expression of the Tnt1 promoter was studied in a gene-for-gene pathosystem, the interaction between tomato and the fungal pathogen Cladosporium fulvum. In compatible interactions, Tnt1 expression is highly induced throughout the leaf regions colonized by the fungus, while in incompatible interactions Tnt1 induction is transient and localized in distinct foci. Tnt1 expression after fungal inoculation parallels the differential activation of tomato defense genes. Tnt1 expression is induced by nonspecific factors of plant or fungal origin present in apoplastic fluids of leaf tissues infected by virulent races of C. fulvum, but is also activated by specific factors resulting from the interaction between fungal avirulence peptides and plant resistance genes. Tnt1 activation by apoplastic fluids containing avirulence peptides of C. fulvum is detected soon after elicitation. These results demonstrate that Tnt1 transcriptional activation correlates with biological responses of tomato to infection by C. fulvum and is mediated through signals originating from both race-specific and non-race-specific perception pathways.
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O'Garro, Leonard W., Harold Gibbs, and Anthony Newton. "Mutation in the avrBs1 Avirulence Gene of Xanthomonas campestris pv. vesicatoria Influences Survival of the Bacterium in Soil and Detached Leaf Tissue." Phytopathology® 87, no. 9 (September 1997): 960–66. http://dx.doi.org/10.1094/phyto.1997.87.9.960.
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The role of the avrBs1 avirulence gene of Xanthomonas campestris pv. vesicatoria in survival of the bacterium was investigated by testing two strains that differ in the structure and function of the gene in 37 different soil types of Barbados and detached leaf tissue of four pepper genotypes. One strain carried a mutation in the avrBs1 gene and lacked avirulence activity, while the other expressed wild-type avrBs1 activity. In 30 to 32 soil types and all leaf tissue tested, the mutant strain persisted longer and more abundantly than the wild-type strain over a 2- to 6-week period. During this time, the mutant strain generally replaced the wild-type strain completely in soil initially infested with a mixture of equal amounts of each strain and by a factor of 6.7 in similarly infested pepper leaves. Nine selected soil factors, namely pH, clay and cation content, and percent nitrogen, carbonates, carbon, K+, Na+, and Ca2+ did not affect bacterial survival significantly.
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JANZAC, BERENGER, FREDERIC FABRE, ALAIN PALLOIX, and BENOIT MOURY. "Constraints on evolution of virus avirulence factors predict the durability of corresponding plant resistances." Molecular Plant Pathology 10, no. 5 (September 2009): 599–610. http://dx.doi.org/10.1111/j.1364-3703.2009.00554.x.
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Neveu, Cédric, Stéphanie Jaubert, Pierre Abad, and Philippe Castagnone-Sereno. "A Set of Genes Differentially Expressed Between Avirulent and Virulent Meloidogyne incognita Near-Isogenic Lines Encode Secreted Proteins." Molecular Plant-Microbe Interactions® 16, no. 12 (December 2003): 1077–84. http://dx.doi.org/10.1094/mpmi.2003.16.12.1077.
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A cDNA-amplification fragment length polymorphism (AFLP)-based strategy has been used to identify genes differentially expressed between two pairs of near-isogenic lines (NIL) of the root-knot nematode Meloidogyne incognita either avirulent or virulent against the tomato Mi resistance gene. Gene expression profiles from infective second-stage juveniles (J2) were compared, and 22 of the 24,025 transcript-derived fragments (TDF) generated proved to be differential, i.e., present in both avirulent NIL and absent in both virulent NIL. Fourteen of the TDF sequences did not show any significant similarity to known proteins, while eight matched reported sequences from nematodes and other invertebrates. The differential expression of nine genes was confirmed by reverse transcription-polymerase chain reaction (RT-PCR) experiments. In situ hybridization conducted with five of the sequences showed that two were specifically expressed in the intestinal cells (HM10 and PM1), one in the subventral esophageal glands (HM1), and two in the dorsal esophageal gland of J2 (HM7 and HM12). Analysis of full-length cDNA sequences revealed the presence of a signal peptide for HM1, HM10, and HM12, indicating that the encoded proteins are putatively secreted. Since secreted products in general and esophageal gland secretions in particular are thought to be among the main M. incognita pathogenicity factors, this result suggests a possible dual role for some of the genes encoding such secretions, i.e., they could be involved in both pathogenicity and virulence or avirulence of these biotrophic parasites.
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Tyler, Brett M. "Inheritance of Avirulence Factors and Restriction Fragment Length Polymorphism Markers in Outcrosses of the OomycetePhytophthora sojae." Molecular Plant-Microbe Interactions 8, no. 4 (1995): 515. http://dx.doi.org/10.1094/mpmi-8-0515.
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Lawrence, G. J. "Flax rust from Linum marginale: pathogenicity reactions on the Linum usitatissimum set of differential varieties." Canadian Journal of Botany 67, no. 11 (November 1, 1989): 3187–91. http://dx.doi.org/10.1139/b89-397.
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Flax rust, Melampsora lini (Ehrenb.) Lév., occurs on Linum marginale Cunn., the only Linum species indigenous to Australia. Evidence suggests that the rust is native to L. marginale and is not a recent introduction. Forty-five isolates from this rust population, collected from 21 locations, were tested for reaction type on the standard set of 28 flax (L. usitatissimum) differential lines. All isolates were avirulent on the majority of differentials and only three clearly different virulence phenotypes were distinguished. This finding contrasts with the results of a companion study in which the same isolates displayed many different virulence phenotypes when tested on a set of L. marginale lines. Two factors apparently contribute to the failure of the L. usitatissimum differentials to detect most of the variation for virulence present in this rust population. First, 10 of the differentials have been reported to possess resistance gene L9 in addition to their designated gene. Since all isolates recognize the L9 gene, these differentials could make no contribution to differentiating between the isolates. Second, many of the L. usitatissimum resistance genes apparently do not occur in L. marginale and with no selection on the rust to conserve or evolve the corresponding virulence genes, the corresponding avirulence genes appear to have become, or remained, fixed in the rust population.
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de Jong, Camiel F., Frank L. W. Takken, Xinzhong Cai, Pierre J. G. M. de Wit, and Matthieu H. A. J. Joosten. "Attenuation of Cf-Mediated Defense Responses at Elevated Temperatures Correlates With a Decrease in Elicitor-Binding Sites." Molecular Plant-Microbe Interactions® 15, no. 10 (October 2002): 1040–49. http://dx.doi.org/10.1094/mpmi.2002.15.10.1040.
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The interaction between the fungal pathogen Cladosporium fulvum and its only host, tomato, is a well-described gene-for-gene system and several resistance (Cf) genes of tomato and matching fungal avirulence (Avr) genes have been characterized. Transgenic tobacco suspension cells expressing Cf genes respond to matching elicitors with typical defense responses, such as medium alkalization and an oxidative burst. We found that this response is attenuated at elevated ambient temperatures. Tomato seedlings expressing both a Cf and the matching Avr gene rapidly die as a result of systemic necrosis at normal temperatures, but are rescued at 33°C. We demonstrate that, at 33°C, the Cf/Avr-mediated induction of defense-related genes is reversibly suppressed. Furthermore, in cell suspensions, the AVR-induced medium alkalization response is slowly suppressed upon incubation at 33°C, but is quickly restored after transfer to lower temperatures. A high-affinity binding site (HABS) for AVR9 is present on plasma membranes isolated from solanaceous plants and has been suggested to act as a co-receptor for AVR9. The amount of AVR9-HABS is 80% reduced in tobacco cell suspensions incubated at 33°C, as compared with cell suspensions incubated at 20°C. Our data suggest that the temperature sensitivity of Cf-mediated defense responses resides at the level of perception of the fungal avirulence factors.
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García-Calderón, Clara B., Meritxell García-Quintanilla, Josep Casadesús, and Francisco Ramos-Morales. "Virulence attenuation in Salmonella enterica rcsC mutants with constitutive activation of the Rcs system." Microbiology 151, no. 2 (February 1, 2005): 579–88. http://dx.doi.org/10.1099/mic.0.27520-0.
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Mutations in rcsC that result in constitutive colanic acid capsule synthesis were obtained in Salmonella enterica serovar Typhimurium. Most rcsC alleles were dominant; however, recessive rcsC alleles were also found, in agreement with the postulated double role (positive and negative) of RcsC on the activation of the RcsB/C phosphorelay system. Salmonella rcsC mutants with constitutive activation of the Rcs system are severely attenuated for virulence in BALB/c mice and their degree of attenuation correlates with the level of Rcs activation. Partial relief of attenuation by a gmm mutation indicates that capsule overproduction is one of the factors leading to avirulence in constitutively activated rcsC mutants.
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Ellison, Damon W., Tina R. Clark, Daniel E. Sturdevant, Kimmo Virtaneva, Stephen F. Porcella, and Ted Hackstadt. "Genomic Comparison of Virulent Rickettsia rickettsii Sheila Smith and Avirulent Rickettsia rickettsii Iowa." Infection and Immunity 76, no. 2 (November 19, 2007): 542–50. http://dx.doi.org/10.1128/iai.00952-07.
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ABSTRACT Rickettsia rickettsii is an obligate intracellular pathogen that is the causative agent of Rocky Mountain spotted fever. To identify genes involved in the virulence of R. rickettsii, the genome of an avirulent strain, R. rickettsii Iowa, was sequenced and compared to the genome of the virulent strain R. rickettsii Sheila Smith. R. rickettsii Iowa is avirulent in a guinea pig model of infection and displays altered plaque morphology with decreased lysis of infected host cells. Comparison of the two genomes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a high degree of sequence identity. A whole-genome alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a total of 143 deletions for the two strains. A subsequent single-nucleotide polymorphism (SNP) analysis comparing Iowa to Sheila Smith revealed 492 SNPs for the two genomes. One of the deletions in R. rickettsii Iowa truncates rompA, encoding a major surface antigen (rickettsial outer membrane protein A [rOmpA]) and member of the autotransporter family, 660 bp from the start of translation. Immunoblotting and immunofluorescence confirmed the absence of rOmpA from R. rickettsii Iowa. In addition, R. rickettsii Iowa is defective in the processing of rOmpB, an autotransporter and also a major surface antigen of spotted fever group rickettsiae. Disruption of rompA and the defect in rOmpB processing are most likely factors that contribute to the avirulence of R. rickettsii Iowa. Genomic differences between the two strains do not significantly alter gene expression as analysis of microarrays revealed only four differences in gene expression between R. rickettsii Iowa and R. rickettsii strain R. Although R. rickettsii Iowa does not cause apparent disease, infection of guinea pigs with this strain confers protection against subsequent challenge with the virulent strain R. rickettsii Sheila Smith.
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Na, Ren, Dan Yu, Dinah Qutob, Jun Zhao, and Mark Gijzen. "Deletion of the Phytophthora sojae Avirulence Gene Avr1d Causes Gain of Virulence on Rps1d." Molecular Plant-Microbe Interactions® 26, no. 8 (August 2013): 969–76. http://dx.doi.org/10.1094/mpmi-02-13-0036-r.
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Phytophthora sojae is an oomycete and a pathogen of soybean that causes root rot. During infection P. sojae delivers effector proteins into host cells to foster disease. However, effector-triggered immunity (ETI) results when pathogen factors are recognized by host resistance (R) proteins. We have now identified the P. sojae Avr1d gene, which encodes a predicted effector protein with the amino acid motif Arg-X-Leu-Arg (RXLR). Genetic mapping of 16 different P. sojae isolates and of a segregating F2 population of 40 individuals shows that the predicted RXLR effector gene Avh6 precisely cosegregates with the Avr1d phenotype. Transient expression assays confirm that Avr1d triggers cell death specifically in Rps1d soybean plants. The Avr1d gene is present in P. sojae strains that are avirulent on Rps1d, whereas the gene is deleted from the genome of virulent strains. Two sequence variants of the Avr1d gene encoding different protein products occur in P. sojae strains, but both are recognized by Rps1d and cause ETI. Liposome binding assays show that Avr1d has affinity for phosphatidylinositol 4-phosphate and that binding can be disrupted by mutation of lysine residues in the carboxy-terminal effector domain of the protein. The identification of Avr1d aids pathogen diagnostics and soybean cultivar development.
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Levic, Jelena, Slavica Stankovic, and Tijana Petrovic. "The determination of Exserohilum turcicum virulence factors in Serbia." Genetika 40, no. 3 (2008): 271–81. http://dx.doi.org/10.2298/gensr0803271l.
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The determination of Exserohilum turcicum virulence factors and resistance responses of three sets of maize inbred lines (four differential, eight isogenic and 22 commercial inbreeds) to three isolates of this pathogen under greenhouse conditions were studied. The maize inbreeds were selected according to previous testing of resistance based on lesion types in 194 inbreeds under field conditions of plant inoculation with the E. turcicum race 0 (designated as the isolate MRI-Et). The standard procedure was applied to obtained isolates MRIZP-1747 and MRIZP-1416 from resistant and susceptible lesion types, respectively. These lesions were developed on the same leaf of a plant of the experimental hybrid no. 163/99 grown in a nursery at Zemun Polje during 1999. The third isolate (MRIZP-1435) was isolated from a leaf sample originating from the location of Srbobran in which the occurrence of northern corn leaf blight (NCLB), caused by Exserohilum turcicum, was intensive. Based upon virulence/avirulence of three isolates of E. turcicum on differential maize inbred lines, it was found out that the isolate MRIZP-1747 could be classified as race 0, whereas isolates MRIZP-1416 and MRIZP-1435 could be classified as race 1. These are the first results that confirm the presence of race 1 of E. turcicum in Serbia. Not including differential lines, 22 and six lines were resistant to race 0 and race 1, respectively, while eight and five lines were resistant and susceptible to both races, respectively. All isogenic lines not containing the Ht gene were susceptible to both races 0 and 1.
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Corbett, Mark, Sam Virtue, Kenneth Bell, Paul Birch, Tom Burr, Lysbeth Hyman, Kathryn Lilley, Susannah Poock, Ian Toth, and George Salmond. "Identification of a New Quorum-Sensing-Controlled Virulence Factor in Erwinia carotovora subsp. atroseptica Secreted via the Type II Targeting Pathway." Molecular Plant-Microbe Interactions® 18, no. 4 (April 2005): 334–42. http://dx.doi.org/10.1094/mpmi-18-0334.
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Two-dimensional polyacrylamide gel electrophoresis of the secreted proteins of Erwinia carotovora subsp. atroseptica revealed alow-abundance protein that was identified by mass spectrometry as a homologue of a Xanthomonas campestris avirulence protein with unknown function. The predicted Svx protein has an N-terminal signal sequence and zinc binding-region signature, and the mature protein is post-translationally modified. A 2D difference gel electrophoresis (DIGE) showed that the protein is secreted by the type II (out) secretion apparatus, which is also responsible for the secretion of the major known virulence factors, PelC and CelV. Transcription of the svx gene is under Nacyl- homoserine lactone-mediated quorum-sensing control. The svx gene was inactivated by transposon insertion. The mutant showed a decrease in virulence in potato plant assays, demonstrating a role for Svx in the pathogenicity of E. carotovora subsp. atroseptica. These results show that Svx is a previously unidentified virulence determinant which is secreted by the out machinery and is regulated by quorum sensing, two systems employed by several other virulence factors. Thus, the type II secretory machine is a conduit for virulence factors other than the main pectinnases and cellulase in E. carotovora subsp. atroseptica.
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Ciesiolka, L. D., T. Hwin, J. D. Gearlds, G. V. Minsavage, R. Saenz, M. Bravo, V. Handley, et al. "Regulation of Expression of Avirulence Gene avrRxv and Identification of a Family of Host Interaction Factors by Sequence Analysis of avrBsT." Molecular Plant-Microbe Interactions® 12, no. 1 (January 1999): 35–44. http://dx.doi.org/10.1094/mpmi.1999.12.1.35.
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Resistance in tomato line Hawaii 7998 as well as in several nonhost plants to Xanthomonas campestris pv. vesicatoria tomato strain (XcvT) is mediated in part by the avirulence gene avrRxv. Analysis of growth of wild-type and avrRxv deletion strains indicates that avrRxv plays a crucial role in the ability of XcvT 92–14 to induce resistance on Hawaii 7998. We used avrRxv reporter gene fusions and Northern (RNA) blot analysis to test several growth environments for inductive potential. We found that avrRxv is constitutively expressed at high levels and that growth in planta, in tobacco conditioned medium, and in hrp-inductive medium XVM2 did not affect the high levels of expression. In addition, hrp structural and regulatory mutant backgrounds had no effect. We mutated the bipartite plant inducible promoter (PIP)-box sequence and found that avrRxv activity appears to be independent of an intact PIP-box element. We present the sequence of the avrRxv homologue called avrBsT and align the six AvrRxv host interaction factor family members including mammalian pathogen virulence factors YopJ and YopP from Yersinia spp. and AvrA from Salmonella typhimurium, and open reading frame Y4LO with unknown function from the symbiont Rhizobium sp.
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Cantila, Aldrin Y., Nur Shuhadah Mohd Saad, Junrey C. Amas, David Edwards, and Jacqueline Batley. "Recent Findings Unravel Genes and Genetic Factors Underlying Leptosphaeria maculans Resistance in Brassica napus and Its Relatives." International Journal of Molecular Sciences 22, no. 1 (December 30, 2020): 313. http://dx.doi.org/10.3390/ijms22010313.
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Among the Brassica oilseeds, canola (Brassica napus) is the most economically significant globally. However, its production can be limited by blackleg disease, caused by the fungal pathogen Lepstosphaeria maculans. The deployment of resistance genes has been implemented as one of the key strategies to manage the disease. Genetic resistance against blackleg comes in two forms: qualitative resistance, controlled by a single, major resistance gene (R gene), and quantitative resistance (QR), controlled by numerous, small effect loci. R-gene-mediated blackleg resistance has been extensively studied, wherein several genomic regions harbouring R genes against L. maculans have been identified and three of these genes were cloned. These studies advance our understanding of the mechanism of R gene and pathogen avirulence (Avr) gene interaction. Notably, these studies revealed a more complex interaction than originally thought. Advances in genomics help unravel these complexities, providing insights into the genes and genetic factors towards improving blackleg resistance. Here, we aim to discuss the existing R-gene-mediated resistance, make a summary of candidate R genes against the disease, and emphasise the role of players involved in the pathogenicity and resistance. The comprehensive result will allow breeders to improve resistance to L. maculans, thereby increasing yield.
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Baltrus, David A., Marc T. Nishimura, Kevin M. Dougherty, Surojit Biswas, M. Shahid Mukhtar, Joana Vicente, Eric B. Holub, and Jeffery L. Dangl. "The Molecular Basis of Host Specialization in Bean Pathovars of Pseudomonas syringae." Molecular Plant-Microbe Interactions® 25, no. 7 (July 2012): 877–88. http://dx.doi.org/10.1094/mpmi-08-11-0218.
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Biotrophic phytopathogens are typically limited to their adapted host range. In recent decades, investigations have teased apart the general molecular basis of intraspecific variation for innate immunity of plants, typically involving receptor proteins that enable perception of pathogen-associated molecular patterns or avirulence elicitors from the pathogen as triggers for defense induction. However, general consensus concerning evolutionary and molecular factors that alter host range across closely related phytopathogen isolates has been more elusive. Here, through genome comparisons and genetic manipulations, we investigate the underlying mechanisms that structure host range across closely related strains of Pseudomonas syringae isolated from different legume hosts. Although type III secretion-independent virulence factors are conserved across these three strains, we find that the presence of two genes encoding type III effectors (hopC1 and hopM1) and the absence of another (avrB2) potentially contribute to host range differences between pathovars glycinea and phaseolicola. These findings reinforce the idea that a complex genetic basis underlies host range evolution in plant pathogens. This complexity is present even in host–microbe interactions featuring relatively little divergence among both hosts and their adapted pathogens.
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Schwartz, Allison R., Robert Morbitzer, Thomas Lahaye, and Brian J. Staskawicz. "TALE-induced bHLH transcription factors that activate a pectate lyase contribute to water soaking in bacterial spot of tomato." Proceedings of the National Academy of Sciences 114, no. 5 (January 18, 2017): E897—E903. http://dx.doi.org/10.1073/pnas.1620407114.
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AvrHah1 [avirulence (avr) gene homologous to avrBs3 and hax2, no. 1] is a transcription activator-like (TAL) effector (TALE) inXanthomonas gardnerithat induces water-soaked disease lesions on fruits and leaves during bacterial spot of tomato. We observe that water from outside the leaf is drawn into the apoplast inX. gardneri-infected, but notX. gardneriΔavrHah1(XgΔavrHah1)-infected, plants, conferring a dark, water-soaked appearance. The pull of water can facilitate entry of additional bacterial cells into the apoplast. Comparing the transcriptomes of tomato infected withX. gardnerivs.XgΔavrHah1revealed the differential up-regulation of two basic helix–loop–helix (bHLH) transcription factors with predicted effector binding elements (EBEs) for AvrHah1. We mined our RNA-sequencing data for differentially up-regulated genes that could be direct targets of the bHLH transcription factors and therefore indirect targets of AvrHah1. We show that two pectin modification genes, a pectate lyase and pectinesterase, are targets of both bHLH transcription factors. Designer TALEs (dTALEs) for the bHLH transcription factors and the pectate lyase, but not for the pectinesterase, complement water soaking when delivered byXgΔavrHah1. By perturbing transcriptional networks and/or modifying the plant cell wall, AvrHah1 may promote water uptake to enhance tissue damage and eventual bacterial egression from the apoplast to the leaf surface. Understanding how disease symptoms develop may be a useful tool for improving the tolerance of crops from damaging disease lesions.
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Wang, Ziyi, Yujiao Du, Suhao Li, Xuewen Xu, and Xuehao Chen. "A Complete Genome Sequence of Podosphaera xanthii Isolate YZU573, the Causal Agent of Powdery Mildew Isolated from Cucumber in China." Pathogens 12, no. 4 (April 6, 2023): 561. http://dx.doi.org/10.3390/pathogens12040561.
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Podosphaera xanthii is a well-known obligate biotrophic pathogen that causes powdery mildew (PM) disease on cucurbitaceous plants and is one of the most important limiting factors for cucumber production worldwide. To better understand the avirulence effector proteins in this species that are known to be involved in host-pathogen interaction, the draft genome assembly of P. xanthii isolate YZU573 from cucumber leaves with symptoms of PM was obtained with a hybrid approach, combining nanopore long-read and llumina paired-end sequencing. The final P. xanthii YZU573 genome assembly of 152.7 Mb consists of 58 contigs, with an N50 value of 0.75 Mb and 6491 predicted protein-coding genes. The effector analysis using the whole-genome sequence information revealed a total of 87 putative effector candidates, and 65 of them had their analogs, whereas the remaining 22 were novel ones. The new P. xanthii genome provides valuable resources to better understand plant-microbe interaction in cucumber PM disease.
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Niks, R. E., and D. Rubiales. "Avirulence factors corresponding to barley genes Pa3 and Pa7 which confer resistance against Puccinia hordei in rust fungi other than P. hordei." Physiological and Molecular Plant Pathology 45, no. 4 (October 1994): 321–31. http://dx.doi.org/10.1016/s0885-5765(05)80062-1.
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Franke, Kathrin, Monika Nguyen, Albert Härtl, Hans-Martin Dahse, Georgia Vogl, Reinhard Würzner, Peter F. Zipfel, Waldemar Künkel, and Raimund Eck. "The vesicle transport protein Vac1p is required for virulence of Candida albicans." Microbiology 152, no. 10 (October 1, 2006): 3111–21. http://dx.doi.org/10.1099/mic.0.29115-0.
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The putative vesicle transport protein Vac1p of the human pathogenic yeast Candida albicans plays an important role in virulence. To determine the cellular functions of Vac1p, a null mutant was generated by sequential disruption of both alleles. The vac1 null mutant strain showed defective endosomal vesicle transport, demonstrating a role of Vac1p in protein transport to the vacuole. Vac1p also contributes to resistance to metal ions, as the null mutant strain was hypersensitive to Cu2+, Zn2+ and Ni2+. In addition, the loss of Vac1p affected several virulence factors of C. albicans. In particular, the vac1 null mutant strain showed defective hyphal growth, even when hyphal formation was induced via different pathways. Furthermore, Vac1p affects chlamydospore formation, adherence to human vaginal epithelial cells, and the secretion of aspartyl proteinases (Saps). Avirulence in a mouse model of systemic infection of the vac1 null mutant strongly suggests that Vac1p of C. albicans is essential for pathogenicity. In summary, the Vac1p protein is required for several cellular pathways, in particular those that control virulence and pathogenicity. Consequently, Vac1p is a novel and interesting target for antifungal drugs.
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Velame, Karinna V. C., Anelita de Jesus Rocha, Mileide dos Santos Ferreira, Fernando Haddad, Vanusia B. Oliveira Amorim, Kátia Nogueira Pestana, Claudia Fortes Ferreira, Saulo Alves Santos de Oliveira, and Edson Perito Amorim. "Evidence of Correlation between Pathogenicity, Avirulence Genes, and Aggressiveness of Fusarium oxysporum f. sp. cubense in Banana “Cavendish” and “Prata” Subgroups." Horticulturae 10, no. 3 (February 27, 2024): 228. http://dx.doi.org/10.3390/horticulturae10030228.
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Fusarium wilt caused by Fusarium oxysporum f. sp. cubense (Foc) is one of the most destructive diseases in banana farming worldwide. Knowledge of the factors of genetic diversity and virulence of the pathogen contributes to the development of resistant cultivars and management strategies based on exclusion. In this study, phenotypic traits such as virulence and aggressiveness in a sample of 52 Foc isolates were analyzed and their relationship to the presence of putative effectors of gene SIX (Secreted in Xylem) pathogenicity homologs was verified. The similarity matrix revealed three isolates that were closest to the standard Foc race 1 strain. Isolates 229A and 218A were selected according to their aggressiveness profile in ‘Grand Naine’ and ‘Prata-Anã’, respectively, to replace the standard isolate of race 1 in the resistance screening process carried out by the breeding program. Two homologs of the SIX8 gene, SIX8a and SIX8b, are present in isolates of Foc from Brazil, and the SIX8b gene correlates with avirulence in the cultivar ‘Grand Naine’ (Cavendish). These results are important to support the banana genetic breeding program by identifying sources of resistance to Foc and contributing to the establishment of the function of SIX effector proteins.
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Hudson, Owen, James C. Fulton, Alexi K. Dong, Nicholas S. Dufault, and Md Emran Ali. "Fusarium oxysporum f. sp. niveum Molecular Diagnostics Past, Present and Future." International Journal of Molecular Sciences 22, no. 18 (September 8, 2021): 9735. http://dx.doi.org/10.3390/ijms22189735.
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Watermelon is an important commercial crop in the Southeastern United States and around the world. However, production is significantly limited by biotic factors including fusarium wilt caused by the hemibiotrophic fungus Fusarium oxysporum forma specialis niveum (Fon). Unfortunately, this disease has increased significantly in its presence over the last several decades as races have emerged which can overcome the available commercial resistance. Management strategies include rotation, improved crop resistance, and chemical control, but early and accurate diagnostics are required for appropriate management. Accurate diagnostics require molecular and genomic strategies due to the near identical genomic sequences of the various races. Bioassays exist for evaluating both the pathogenicity and virulence of an isolate but are limited by the time and resources required. Molecular strategies are still imperfect but greatly reduce the time to complete the diagnosis. This article presents the current state of the research surrounding races, both how races have been detected and diagnosed in the past and future prospects for improving the system of differentiation. Additionally, the available Fon genomes were analyzed using a strategy previously described in separate formae speciales avirulence gene association studies in Fusarium oxysporum races.
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Kharel, Aayushree, Md Tohidul Islam, James Rookes, and David Cahill. "How to Unravel the Key Functions of Cryptic Oomycete Elicitin Proteins and Their Role in Plant Disease." Plants 10, no. 6 (June 12, 2021): 1201. http://dx.doi.org/10.3390/plants10061201.
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Pathogens and plants are in a constant battle with one another, the result of which is either the restriction of pathogen growth via constitutive or induced plant defense responses or the pathogen colonization of plant cells and tissues that cause disease. Elicitins are a group of highly conserved proteins produced by certain oomycete species, and their sterol binding ability is recognized as an important feature in sterol–auxotrophic oomycetes. Elicitins also orchestrate other aspects of the interactions of oomycetes with their plant hosts. The function of elicitins as avirulence or virulence factors is controversial and is dependent on the host species, and despite several decades of research, the function of these proteins remains elusive. We summarize here our current understanding of elicitins as either defense-promoting or defense-suppressing agents and propose that more recent approaches such as the use of ‘omics’ and gene editing can be used to unravel the role of elicitins in host–pathogen interactions. A better understanding of the role of elicitins is required and deciphering their role in host–pathogen interactions will expand the strategies that can be adopted to improve disease resistance and reduce crop losses.
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Delourme, R., M. L. Pilet-Nayel, M. Archipiano, R. Horvais, X. Tanguy, T. Rouxel, H. Brun, M. Renard, and M. H. Balesdent. "A Cluster of Major Specific Resistance Genes to Leptosphaeria maculans in Brassica napus." Phytopathology® 94, no. 6 (June 2004): 578–83. http://dx.doi.org/10.1094/phyto.2004.94.6.578.
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Two types of genetic resistance to Leptosphaeria maculans usually are distinguished in Brassica napus: qualitative, total resistance expressed at the seedling stage and quantitative, partial resistance expressed at the adult plant stage. The latter is under the control of many genetic factors that have been mapped through quantitative trait loci (QTL) studies using ‘Darmor’ resistance. The former usually is ascribed to race-specific resistance controlled by single resistance to L. maculans (Rlm) genes. Three B. napus-originating specific Rlm genes (Rlm1, Rlm2, and Rlm4) previously were characterized. Here, we report on the genetic identification of two novel resistance genes, Rlm3 and Rlm7, corresponding to the avirulence genes AvrLm3 and AvrLm7. The identification of a novel L. maculans- B. napus specific interaction allowed the detection of another putative new specific resistance gene, Rlm9. The resistance genes were mapped in two genomic regions on LG10 and LG16 linkage groups. A cluster of five resistance genes (Rlm1, Rlm3, Rlm4, Rlm7, and Rlm9) was strongly suggested on LG10. The relation between all these specific resistance genes and their potential role in adult-plant field resistance is discussed. These two Rlm-carrying regions do not correspond to major QTL for Darmor quantitative resistance.
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Thordal-Christensen, Hans. "A holistic view on plant effector-triggered immunity presented as an iceberg model." Cellular and Molecular Life Sciences 77, no. 20 (April 10, 2020): 3963–76. http://dx.doi.org/10.1007/s00018-020-03515-w.
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Abstract The immune system of plants is highly complex. It involves pattern-triggered immunity (PTI), which is signaled and manifested through branched multi-step pathways. To counteract this, pathogen effectors target and inhibit individual PTI steps. This in turn can cause specific plant cytosolic nucleotide-binding leucine-rich repeat (NLR) receptors to activate effector-triggered immunity (ETI). Plants and pathogens have many genes encoding NLRs and effectors, respectively. Yet, only a few segregate genetically as resistance (R) genes and avirulence (Avr) effector genes in wild-type populations. In an attempt to explain this contradiction, a model is proposed where far most of the NLRs, the effectors and the effector targets keep one another in a silent state. In this so-called “iceberg model”, a few NLR-effector combinations are genetically visible above the surface, while the vast majority is hidden below. Besides, addressing the existence of many NLRs and effectors, the model also helps to explain why individual downregulation of many effectors causes reduced virulence and why many lesion-mimic mutants are found. Finally, the iceberg model accommodates genuine plant susceptibility factors as potential effector targets.
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Knoop, V., B. Staskawicz, and U. Bonas. "Expression of the avirulence gene avrBs3 from Xanthomonas campestris pv. vesicatoria is not under the control of hrp genes and is independent of plant factors." Journal of Bacteriology 173, no. 22 (1991): 7142–50. http://dx.doi.org/10.1128/jb.173.22.7142-7150.1991.
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VandeWoude, Sue, and Cristian Apetrei. "Going Wild: Lessons from Naturally Occurring T-Lymphotropic Lentiviruses." Clinical Microbiology Reviews 19, no. 4 (October 2006): 728–62. http://dx.doi.org/10.1128/cmr.00009-06.
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SUMMARY Over 40 nonhuman primate (NHP) species harbor species-specific simian immunodeficiency viruses (SIVs). Similarly, more than 20 species of nondomestic felids and African hyenids demonstrate seroreactivity against feline immunodeficiency virus (FIV) antigens. While it has been challenging to study the biological implications of nonfatal infections in natural populations, epidemiologic and clinical studies performed thus far have only rarely detected increased morbidity or impaired fecundity/survival of naturally infected SIV- or FIV-seropositive versus -seronegative animals. Cross-species transmissions of these agents are rare in nature but have been used to develop experimental systems to evaluate mechanisms of pathogenicity and to develop animal models of HIV/AIDS. Given that felids and primates are substantially evolutionarily removed yet demonstrate the same pattern of apparently nonpathogenic lentiviral infections, comparison of the biological behaviors of these viruses can yield important implications for host-lentiviral adaptation which are relevant to human HIV/AIDS infection. This review therefore evaluates similarities in epidemiology, lentiviral genotyping, pathogenicity, host immune responses, and cross-species transmission of FIVs and factors associated with the establishment of lentiviral infections in new species. This comparison of consistent patterns in lentivirus biology will expose new directions for scientific inquiry for understanding the basis for virulence versus avirulence.
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Moscou, Matthew J., Nick Lauter, Rico A. Caldo, Dan Nettleton, and Roger P. Wise. "Quantitative and Temporal Definition of the Mla Transcriptional Regulon During Barley–Powdery Mildew Interactions." Molecular Plant-Microbe Interactions® 24, no. 6 (June 2011): 694–705. http://dx.doi.org/10.1094/mpmi-09-10-0211.
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Barley Mildew resistance locus a (Mla) is a major determinant of immunity to the powdery mildew pathogen, Blumeria graminis f. sp. hordei. Alleles of Mla encode cytoplasmic- and membrane-localized coiled-coil, nucleotide binding site, leucine-rich repeat proteins that mediate resistance when complementary avirulence effectors (AVRa) are present in the pathogen. Presence of an appropriate AVRa protein triggers nuclear relocalization of MLA, in which MLA binds repressing host transcription factors. Timecourse expression profiles of plants harboring Mla1, Mla6, and Mla12 wild-type alleles versus paired loss-of-function mutants were compared to discover conserved transcriptional targets of MLA and downstream signaling cascades. Pathogen-dependent gene expression was equivalent or stronger in susceptible plants at 20 h after inoculation (HAI) and was attenuated at later timepoints, whereas resistant plants exhibited a time-dependent strengthening of the transcriptional response, increasing in both fold change and the number of genes differentially expressed. Deregulation at 20 HAI implicated 16 HAI as a crucial point in determining the future trajectory of this interaction and was interrogated by quantitative analysis. In total, 28 potential transcriptional targets of the MLA regulon were identified. These candidate targets possess a diverse set of predicted functions, suggesting that multiple pathways are required to mediate the hypersensitive reaction.
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Chiba, Soutaro, Hideki Kondo, Masaki Miyanishi, Ida Bagus Andika, Chenggui Han, and Tetsuo Tamada. "The Evolutionary History of Beet necrotic yellow vein virus Deduced from Genetic Variation, Geographical Origin and Spread, and the Breaking of Host Resistance." Molecular Plant-Microbe Interactions® 24, no. 2 (February 2011): 207–18. http://dx.doi.org/10.1094/mpmi-10-10-0241.
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Beet necrotic yellow vein virus (BNYVV) is an economically important pathogen of sugar beet and has been found worldwide, probably as the result of recent worldwide spread. The BNYVV genome consists of four or five RNA components. Here, we report analysis of sequence variation in the RNA3-p25, RNA4-p31, RNA2-CP, and RNA5-p26 genes of 73 worldwide isolates. The RNA3-p25 gene encodes virulence and avirulence factors. These four sets of gene sequences each fell into two to four groups, of which the three groups of p25 formed eight subgroups with different geographical distributions. Each of these subgroup isolates (strains) could have arisen from four original BNYVV population and their mixed infections. The genetic diversity for BNYVV was relatively small. Selection pressure varied greatly depending on the BNYVV gene and geographical location. Isolates of the Italy strain, in which p25 was subject to the strongest positive selection, were able to overcome the Rz1-host resistance gene to differing degrees, whereas other geographically limited strains could not. Resistance-breaking variants were generated by p25 amino acid changes at positions 67 and 68. Our studies suggest that BNYVV originally evolved in East Asia and has recently become a pathogen of cultivated sugar beet followed by the emergence of new resistance-breaking variants.
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Simsek, Senay, Tuula Ojanen-Reuhs, Samuel B. Stephens, and Bradley L. Reuhs. "Strain-Ecotype Specificity in Sinorhizobium meliloti-Medicago truncatula Symbiosis Is Correlated to Succinoglycan Oligosaccharide Structure." Journal of Bacteriology 189, no. 21 (August 31, 2007): 7733–40. http://dx.doi.org/10.1128/jb.00739-07.
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ABSTRACT Molecular signals, including Nod factors and succinoglycan, are necessary for the establishment of nitrogen-fixing nodules (Fix+) in Medicago truncatula-Sinorhizobium meliloti symbiosis. This report shows that M. truncatula-S. meliloti interactions involve ecotype-strain specificity, as S. meliloti Rm41 and NRG247 are Fix+ (compatible) on M. truncatula A20 and Fix− (incompatible) on M. truncatula A17, the Fix phenotypes are reversed with S. meliloti NRG185 and NRG34, and there is a correlation between the host specificity and succinoglycan oligosaccharide structure. S. meliloti NRG185 produces oligosaccharides that are almost fully succinylated, with two succinate groups per subunit, whereas the oligosaccharides produced by S. meliloti Rm41 include many nonsuccinylated subunits, as well as subunits with a single succinate group and others with malate. The results of this study demonstrated the following: (i) incompatibility is not a consequence of an avirulence factor or lack of Nod factor activity; (ii) the Fix+ phenotypes are succinoglycan dependent; (iii) there is structural variability in the succinoglycan oligosaccharide populations between S. meliloti strains; (iv) the structural nature of the succinoglycan oligosaccharides is correlated to compatibility; most importantly, (v) an S. meliloti Rm41 derivative, carrying exo genes from an M. truncatula A17-compatible strain, produced a modified population of succinoglycan oligosaccharides (similar to the donor strain) and was Fix+ on A17.
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Tesfamariam, Mahelat, Picabo Binette, Diane Cockrell, Paul A. Beare, Robert A. Heinzen, Carl Shaia, and Carrie Mae Long. "Characterization of Coxiella burnetii Dugway Strain Host-Pathogen Interactions In Vivo." Microorganisms 10, no. 11 (November 15, 2022): 2261. http://dx.doi.org/10.3390/microorganisms10112261.
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Coxiella burnetii is a Gram-negative, intracellular bacterium that causes the zoonosis Q fever. Among the many natural isolates of C. burnetii recovered from various sources, the Dugway group exhibits unique genetic characteristics, including the largest C. burnetii genomes. These strains were isolated during 1954–1958 from wild rodents from the Utah, USA desert. Despite retaining phase I lipopolysaccharide and the type 4B secretion system, two critical virulence factors, avirulence has been reported in a guinea pig infection model. Using guinea pig models, we evaluated the virulence, whole-cell vaccine (WCV) efficacy, and post-vaccination hypersensitivity (PVH) potential of a representative Dugway strain. Consistent with prior reports, Dugway appeared to be highly attenuated compared to a virulent strain. Indeed, Dugway-infected animals showed similarly low levels of fever, body weight loss, and splenomegaly like Nine Mile II-infected animals. When compared to a human Q fever vaccine, QVax®, Dugway WCV exhibited analogous protection against a heterologous Nine Mile I challenge. PVH was investigated in a skin-testing model which revealed significantly decreased maximum erythema in Dugway Δdot/icm WCV-skin-tested animals compared to that of QVax®. These data provide insight into this unique bacterial strain and implicate its potential use as a mutated WCV candidate.
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Paulin, Susan M., Patricia R. Watson, Annette R. Benmore, Mark P. Stevens, Philip W. Jones, Bernardo Villarreal-Ramos, and Timothy S. Wallis. "Analysis of Salmonella enterica Serotype-Host Specificity in Calves: Avirulence of S. enterica Serotype Gallinarum Correlates with Bacterial Dissemination from Mesenteric Lymph Nodes and Persistence In Vivo." Infection and Immunity 70, no. 12 (December 2002): 6788–97. http://dx.doi.org/10.1128/iai.70.12.6788-6797.2002.
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ABSTRACT Host and bacterial factors that determine whether Salmonella serotypes remain restricted to the gastrointestinal tract or penetrate beyond the mucosa and cause systemic disease remain largely undefined. Here, factors influencing Salmonella host specificity in calves were assessed by characterizing the pathogenesis of different serotypes. Salmonella enterica serotype Dublin was highly virulent intravenously, whereas S. enterica serotype Choleraesuis was moderately virulent. Both serotypes were virulent in calves infected orally. In contrast, S. enterica serotypes Gallinarum and Abortusovis were avirulent by either route. Serotypes Dublin, Gallinarum, and Abortusovis colonized the intestinal tract 24 h after oral inoculation, yet only serotype Dublin was consistently recovered from systemic tissues. Serotypes Dublin and Gallinarum invaded bovine intestines in greater numbers and induced greater enteropathogenic responses than serotypes Choleraesuis and Abortusovis. However, only serotype Dublin was able to persist within the intestinal mucosa, and use of a novel cannulation model demonstrated that serotype Dublin was able to pass through the mesenteric lymph nodes in greater numbers than serotype Gallinarum. Together, these results suggest that initial interactions with the intestinal mucosa do not correlate with host specificity, although persistence within tissues and translocation via efferent lymphatics appear to be crucial for the induction of bovine salmonellosis.
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Timko, Michael P., Kan Huang, and Karolina E. Lis. "Host Resistance and Parasite Virulence in Striga–Host Plant Interactions: A Shifting Balance of Power." Weed Science 60, no. 2 (June 2012): 307–15. http://dx.doi.org/10.1614/ws-d-11-00039.1.
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The witchweeds, members of the genus Striga, are noxious and persistent pests in farmers' fields and serious constraints to crop productivity throughout Africa, India, and Southeast Asia. Among the primary hosts for Striga are the major cereals (maize, sorghum, rice, and millet) and grain legumes (cowpea) that are important food staples worldwide. The negative impact of parasitic plants on crop productivity increases globally each year, and their potential for affecting domestic agriculture looms larger as the movement of seed resources expands on a global scale. At the present time there is a limited understanding of how Striga and other parasitic plants select a suitable host and overcome the innate defense responses of the host in order to complete their life-cycle. In the grasses most reported resistance to Striga appears to be polygenic with a large genotype by environment interaction. In contrast, resistance to S. gesnerioides in cowpea is conferred by single dominant genes functioning in a race-specific manner suggesting that a gene-for-gene mechanism similar to effector-triggered immunity (ETI) described in other host–pathogen interactions is likely operating in these parasite-host associations. A hallmark of ETI is the direct or indirect recognition of parasite-derived avirulence (Avr) factors and other effectors that interfere with plant innate immunity by host sensors (or R proteins) leading to activation of defense responses. The recent cloning and functional characterization of a race-specific R gene from cowpea encoding a canonical coiled-coil (CC)-nucleotide binding site (NBS)-leucine-rich repeat (LRR) type R-protein opens the door for further exploration of the mechanism of host resistance and provides a focal point for studies aimed at uncovering the molecular and genetic factors underlying parasite virulence and host selection. The potential for the development of novel strategies for parasite control and eradication based on parasite virulence factors is discussed.
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Ji, Zhiyuan, Wei Guo, Xifeng Chen, Chunlian Wang, and Kaijun Zhao. "Plant Executor Genes." International Journal of Molecular Sciences 23, no. 3 (January 28, 2022): 1524. http://dx.doi.org/10.3390/ijms23031524.
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Executor (E) genes comprise a new type of plant resistance (R) genes, identified from host–Xanthomonas interactions. The Xanthomonas-secreted transcription activation-like effectors (TALEs) usually function as major virulence factors, which activate the expression of the so-called “susceptibility” (S) genes for disease development. This activation is achieved via the binding of the TALEs to the effector-binding element (EBE) in the S gene promoter. However, host plants have evolved EBEs in the promoters of some otherwise silent R genes, whose expression directly causes a host cell death that is characterized by a hypersensitive response (HR). Such R genes are called E genes because they trap the pathogen TALEs in order to activate expression, and the resulting HR prevents pathogen growth and disease development. Currently, deploying E gene resistance is becoming a major component in disease resistance breeding, especially for rice bacterial blight resistance. Currently, the biochemical mechanisms, or the working pathways of the E proteins, are still fuzzy. There is no significant nucleotide sequence homology among E genes, although E proteins share some structural motifs that are probably associated with the signal transduction in the effector-triggered immunity. Here, we summarize the current knowledge regarding TALE-type avirulence proteins, E gene activation, the E protein structural traits, and the classification of E genes, in order to sharpen our understanding of the plant E genes.
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Lokossou, Anoma A., Hendrik Rietman, Miqia Wang, Pavel Krenek, Hanneke van der Schoot, Betty Henken, Roel Hoekstra, et al. "Diversity, Distribution, and Evolution of Solanum bulbocastanum Late Blight Resistance Genes." Molecular Plant-Microbe Interactions® 23, no. 9 (September 2010): 1206–16. http://dx.doi.org/10.1094/mpmi-23-9-1206.
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Knowledge on the evolution and distribution of late blight resistance genes is important for a better understanding of the dynamics of these genes in nature. We analyzed the presence and allelic diversity of the late blight resistance genes Rpi-blb1, Rpi-blb2, and Rpi-blb3, originating from Solanum bulbocastanum, in a set of tuber-bearing Solanum species comprising 196 different taxa. The three genes were only present in some Mexican diploid as well as polyploid species closely related to S. bulbocastanum. Sequence analysis of the fragments obtained from the Rpi-blb1 and Rpi-blb3 genes suggests an evolution through recombinations and point mutations. For Rpi-blb2, only sequences identical to the cloned gene were found in S. bulbocastanum accessions, suggesting that it has emerged recently. The three resistance genes occurred in different combinations and frequencies in S. bulbocastanum accessions and their spread is confined to Central America. A selected set of genotypes was tested for their response to the avirulence effectors IPIO-2, Avr-blb2, and Pi-Avr2, which interact with Rpi-blb1, Rpi-blb2, and Rpi-blb3, respectively, as well as by disease assays with a diverse set of isolates. Using this approach, some accessions could be identified that contain novel, as yet unknown, late blight resistance factors in addition to the Rpi-blb1, Rpi-blb2, and Rpi-blb3 genes.
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Zhang, Na, Xinyang Li, Liangping Ming, Wenda Sun, Xiaofang Xie, Cailing Zhi, Xiaofan Zhou, Yanhua Wen, Zhibin Liang, and Yizhen Deng. "Comparative Genomics and Pathogenicity Analysis of Three Fungal Isolates Causing Barnyard Grass Blast." Journal of Fungi 10, no. 12 (December 13, 2024): 868. https://doi.org/10.3390/jof10120868.
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Barnyard grass is one of the most serious rice weeds, often growing near paddy fields and therefore potentially serving as a bridging host for the rice blast fungus. In this study, we isolated three fungal strains from diseased barnyard grass leaves in a rice field. Using a pathogenicity assay, we confirmed that they were capable of causing blast symptoms on barnyard grass and rice leaves to various extents. Based on morphology characterization and genome sequence analyses, we confirmed that these three strains were Epicoccum sorghinum (SCAU-1), Pyricularia grisea (SCAU-2), and Exserohilum rostratum (SCAU-6). The established Avirulence (Avr) genes Avr-Pia, Avr-Pita2, and ACE1 were detected by PCR amplification in SCAU-2, but not in SCAU-1 or SCAU-6. Furthermore, the whole-genome sequence analysis helped to reveal the genetic variations and potential virulence factors relating to the host specificity of these three fungal pathogens. Based on the evolutionary analysis of single-copy orthologous proteins, we found that the genes encoding glycoside hydrolases, carbohydrate esterases, oxidoreductase, and multidrug transporters in SCAU-1 and SCAU-6 were expanded, while expansion in SCAU-2 was mainly related to carbohydrate esterases. In summary, our study provides clues to understand the pathogenic mechanisms of fungal isolates from barnyard grass with the potential to cause rice blast.
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Wen, R. H., B. Khatabi, T. Ashfield, M. A. Saghai Maroof, and M. R. Hajimorad. "The HC-Pro and P3 Cistrons of an Avirulent Soybean mosaic virus Are Recognized by Different Resistance Genes at the Complex Rsv1 Locus." Molecular Plant-Microbe Interactions® 26, no. 2 (February 2013): 203–15. http://dx.doi.org/10.1094/mpmi-06-12-0156-r.
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The complex Rsv1 locus in soybean plant introduction (PI) ‘PI96983’ confers extreme resistance (ER) against Soybean mosaic virus (SMV) strain N but not SMV-G7 and SMV-G7d. Both the SMV helper-component proteinase (HC-Pro) and P3 cistrons can serve as avirulence factors recognized by Rsv1. To understand the genetics underlying recognition of the two cistrons, we have utilized two soybean lines (L800 and L943) derived from crosses between PI96983 (Rsv1) and Lee68 (rsv1) with distinct recombination events within the Rsv1 locus. L800 contains a single PI96983-derived member (3gG2) of an Rsv1-associated subfamily of nucleotide-binding leucine-rich repeat (NB-LRR) genes. In contrast, although L943 lacks 3gG2, it contains a suite of five other NB-LRR genes belonging to the same family. L800 confers ER against SMV-N whereas L943 allows limited replication at the inoculation site. SMV-N-derived chimeras containing HC-Pro from SMV-G7 or SMV-G7d gained virulence on L943 but not on L800 whereas those with P3 replacement gained virulence on L800 but not on L943. In reciprocal experiments, SMV-G7- and SMV-G7d-derived chimeras with HC-Pro replacement from SMV-N lost virulence on L943 but retained virulence on L800 whereas those with P3 replacement lost virulence on L800 while remaining virulent on L943. These data demonstrate that distinct resistance genes at the Rsv1 locus, likely belonging to the NB-LRR class, mediate recognition of HC-Pro and P3.
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Tamizi, Amin-Asyraf, Norliza Abu-Bakar, Aimera-Farhana Samsuddin, Lina Rozano, Rohaiza Ahmad-Redzuan, and Abdul-Munir Abdul-Murad. "Characterisation and Mutagenesis Study of An Alternative Sigma Factor Gene (hrpL) from Erwinia mallotivora Reveal Its Central Role in Papaya Dieback Disease." Biology 9, no. 10 (October 3, 2020): 323. http://dx.doi.org/10.3390/biology9100323.
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The alternative sigma (σ) factor E, RpoE or HrpL, has been reported to be involved in stress- and pathogenicity-related transcription initiation in Escherichia coli and many other Gram-negative bacteria, including Erwinia spp. and Pseudomonas spp. A previous study identified the hrpL/rpoE transcript as one of the significant differentially expressed genes (DEGs) during early E. mallotivora infection in papaya and those data serve as the basis of the current project. Here, the full coding DNA sequence (CDS) of hrpL from E. mallotivora (EmhrpL) was determined to be 549 bp long, and it encoded a 21.3 kDa HrpL protein that possessed two highly conserved sigma-70 (σ70) motifs—σR2 and σR4. Nucleotide sequence alignment revealed the hrpL from E. mallotivora shared high sequence similarity to rpoE/hrpL from E. tracheiphila (83%), E. pyrifoliae (81%), and E. tasmaniensis (80%). Phylogenetics analysis indicated hrpL from E. mallotivora to be monophyletic with rpoEs/hrpLs from Pantoea vagans, E. herbicola, and E. tracheiphila. Structural analysis postulated that the E. mallotivora’s alternative σ factor was non-transmembranic and was an extracytoplasmic function (ECF) protein—characteristics shared by other σ factors in different bacterial species. Notably, the protein–protein interaction (PPI) study through molecular docking suggested the σ factor could be possibly inhibited by an anti-σ. Finally, a knockout of hrpL in E. mallotivora (ΔEmhrpL) resulted in avirulence in four-month-old papaya plants. These findings have revealed that the hrpL is a necessary element in E. mallotivora pathogenicity and also predicted that the gene can be inhibited by an anti-σ.
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Hendrickson, Erik L., Pablo Guevera, Alejandro Peñaloza-Vàzquez, Jing Shao, Carol Bender, and Frederick M. Ausubel. "Virulence of the Phytopathogen Pseudomonas syringae pv. Maculicola Is rpoN Dependent." Journal of Bacteriology 182, no. 12 (June 15, 2000): 3498–507. http://dx.doi.org/10.1128/jb.182.12.3498-3507.2000.
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ABSTRACT We cloned the rpoN (ntrA andglnF) gene encoding ς54 from the phytopathogen Pseudomonas syringae pv. maculicola strain ES4326. The P. syringae ES4326 rpoN gene complemented Pseudomonas aeruginosa, Escherichia coli, and Klebsiella aerogenes rpoN mutants for a variety of rpoN mutant phenotypes, including the inability to utilize nitrate as sole nitrogen source. DNA sequence analysis of the P. syringae ES4326 rpoN gene revealed that the deduced amino acid sequence was most similar (86% identity; 95% similarity) to the ς54 protein encoded by thePseudomonas putida rpoN gene. A marker exchange protocol was used to construct an ES4326 rpoN insertional mutation,rpoN::Kmr. In contrast to wild-type ES4326, ES4326 rpoN::Kmr was nonmotile and could not utilize nitrate, urea, C4-dicarboxylic acids, several amino acids, or concentrations of ammonia below 2 mM as nitrogen sources.rpoN was essential for production of the phytotoxin coronatine and for expression of the structural genes encoding coronamic acid. In addition, ES4326rpoN::Kmr did not multiply or elicit disease symptoms when infiltrated into Arabidopsis thalianaleaves, did not elicit the accumulation of severalArabidopsis defense-related mRNAs, and did not elicit a hypersensitive response (HR) when infiltrated into tobacco (Nicotiana tabacum) leaves. Furthermore, whereas P. syringae ES4326 carrying the avirulence gene avrRpt2elicited an HR when infiltrated into Arabidopsis ecotype Columbia leaves, ES4326 rpoN::Kmrcarrying avrRpt2 elicited no response. Constitutive expression of ES4326 hrpL in ES4326rpoN::Kmr partially restored defense-related mRNA accumulation, showing a direct role for thehrp cluster in host defense gene induction in a compatible host-pathogen interaction. However, constitutive expression ofhrpL in ES4326 rpoN::Kmrdid not restore coronatine production, showing that coronatine biosynthesis requires factors other than hrpL.
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Shafikova, T. N., and Yu V. Omelichkina. "Evolution of views on plant immunity: from Flor’s “gene-for-gene” theory to the “zig-zag model” developed by Jones and Dangl." Proceedings of Universities. Applied Chemistry and Biotechnology 10, no. 3 (October 8, 2020): 424–38. http://dx.doi.org/10.21285/2227-2925-2020-10-3-424-438.
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The study of plant defence mechanisms in response to pathogens in the mid-20th century resulted in Harold Flor’s gene-for-gene interaction hypothesis, which became recognised as central to the study of phytoimmunity. According to this theory, the outcome of interactions in plant – pathogen phytopathosystems – i.e. compatibility or incompatibility – is controlled genetically in interacting organisms and determined by the presence of specific genes in both pathogen and plant: resistance genes in the plant and avirulence genes in pathogen. The latest achievements in phytoimmunology, obtained with the help of modern molecular biology and bioinformatics methods, have made a significant contribution to the classical understanding of plant immunity and provided grounds for a modern concept of phytoimmunity consisting in the “zig-zag model” developed by Jonathan Jones and Jefferey Dangl. Plant immunity is currently understood as being determined by an innate multi-layer immune system involving various structures and mechanisms of specific and non-specific immunity. Recognition by plant membrane receptors of conservative molecular patterns associated with microorganisms, as well as molecules produced during cell wall disruption by pathogen hydrolytic enzymes forms a basic non-specific immune response in the plant. Detection of pathogen effector molecules by plant intra-cellular receptors triggers a specific effector-triggered immunity, resulting in the development of the hypersensitive response, systemic resistance and immune memory of the plant. Virulence factors and pathogen attack strategies on the one hand, and mechanisms of plant immune protection on the other, are the result of one form of constant co-evolution, often termed an “evolutionary arms race”. This paper discusses the main principles of Flor's classical “gene-for-gene interaction” theory as well as the molecular-genetic processes of plant innate immunity, their mechanisms and participants in light of contemporary achievements in phytoimmunology.
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Adhikari, Tika B., Jianfa Bai, Steven W. Meinhardt, Suraj Gurung, Mary Myrfield, Jaimin Patel, Shaukat Ali, Neil C. Gudmestad, and Jack B. Rasmussen. "Tsn1-Mediated Host Responses to ToxA from Pyrenophora tritici-repentis." Molecular Plant-Microbe Interactions® 22, no. 9 (September 2009): 1056–68. http://dx.doi.org/10.1094/mpmi-22-9-1056.
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The toxin sensitivity gene Tsn1 interacts with Ptr ToxA (ToxA), a host-selective toxin produced by the necrotrophic fungus Pyrenophora tritici-repentis. The molecular mechanisms associated with cell death in sensitive wheat cultivars following ToxA application are not well understood. To address this question, we used the Affymetrix GeneChip Wheat Genome Array to compare gene expression in a sensitive wheat cultivar possessing the Tsn1 gene with the insensitive wheat cv. Nec103, which lacks the Tsn1 gene. This analysis was performed at early timepoints after infiltration with ToxA (e.g., 0.5 to 12 h postinfiltration [hpi]); at this time, ToxA is known to internalize into mesophyll cells without visible cell death symptoms. Gene expression also was monitored at later timepoints (24 to 48 hpi), when ToxA causes extensive damage in cellular compartments and visible cell death. At both early and late timepoints, numerous defense-related genes were induced (2- to 197-fold increases) and included genes involved in the phenylpropanoid pathway, lignification, and the production of reactive oxygen species (ROS). Furthermore, a subset of host genes functioning in signal transduction, metabolism, and as transcription factors was induced as a consequence of the Tsn1–ToxA interaction. Nine genes known to be involved in the host defense response and signaling pathways were selected for analysis by quantitative real-time polymerase chain reaction, and the expression profiles of these genes confirmed the results obtained in microarray experiments. Histochemical analyses of a sensitive wheat cultivar showed that H2O2 was present in leaves undergoing cell death, indicating that ROS signaling is a major event involved in ToxA-mediated cell death. The results suggest that recognition of ToxA via Tsn1 triggers transcriptional reprogramming events similar to those reported for avirulence–resistance gene interactions, and that host-derived genes play an important role in the modulation of susceptibility to P. tritici-repentis.