An avrPto/avrPtoB Mutant of Pseudomonas syringae pv. tomato DC3000 Does Not Elicit Pto-Mediated Resistance and Is Less Virulent on Tomato

Lin, Nai-Chun; Martin, Gregory B.

doi:10.1094/mpmi-18-0043

Cited by 134 publications

(151 citation statements)

References 50 publications

Supporting

Mentioning

138

Contrasting

Order By: Relevance

“…This discovery is consistent with observations that single DC3000 deletion mutants of AvrPto or AvrPtoB exhibit similar levels of virulence 99 . AvrPtoB E3 ubiquitin ligase activity is probably not required for the suppression of basal defences, because mutations in the residues that are required for AvrPtoB E3 ubiquitin ligase activity and anti-PCD function do not abrogate the capability of AvrPtoB to suppress basal defences 42,76 .…”

Section: Bacterial Suppression Of Hr-based Pcdsupporting

confidence: 91%

Bacterial elicitation and evasion of plant innate immunity

Abramovitch

Anderson

Martin

2006

Nat Rev Mol Cell Biol

Self Cite

375

285

View full text Add to dashboard Cite

Recent research on plant responses to bacterial attack has identified extracellular and intracellular host receptors that recognize conserved pathogen-associated molecular patterns and more specialized virulence proteins, respectively. These findings have shed light on our understanding of the molecular mechanisms by which bacteria elicit host defences and how pathogens have evolved to evade or suppress these defences.Plants are a rich source of nutrients and water for microbes, and they are infected by many bacterial pathogens from both the Proteobacteria and Actinobacteria phyla (Supplementary information 1 (table)). Because of their broad host range, serious economic consequences and experimental tractability, the most intensively studied bacteria are members of the Proteobacteria phylum (such as Agrobacterium, Erwinia, Pseudomonas, Ralstonia and Xanthomonas) [1][2][3][4] . These pathogens are spread by wind, rain, insects or cultivation practices. They enter plant tissues either by wounds or through natural openings such as lenticels, hydathodes or stomata 5 , and they occupy the inter cellular spaces (apoplast) of various plant tissues or the xylem.Plant-pathogenic members of the Proteobacteria cause diverse disease symptoms, including specks, spots, blights, wilts, galls and cankers, and they can cause host-cell death in roots, leaves, flowers, fruits, stems and tubers (FIG. 1). These symptoms affect both yield and quality of agricultural crops and bacterial diseases can have serious economic, social and even political consequences [6][7][8] . Control of bacterial diseases is only partially effective and consists of copper-based sprays, antibiotics, biocontrol strategies, large-scale removal of infected plants and, most importantly, host genetic resistance 5 . Therefore, research on bacterial diseases of plants helps to elucidate fundamental aspects of microbial pathogenesis and associated host responses and also to develop more effective and sustainable disease-control methods.Correspondence to G.B.M. gbm7@cornell.edu. Competing interests statementThe authors declare no competing financial interests. DATABASES NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptPlant-pathogenic bacteria use virulence strategies that are either specialized to plant tissues or are broadly conserved among pathogens of both plants and animals (FIG. 1). Bacterial virulence is manifested as increases in the rate of growth or final population size, as well as by enhanced disease symptoms, which promote the spread of the pathogen through the plant or the broader environment.Unlike mammals, plants have a complex cell wall that bacteria must surmount to gain access to water and nutrients. Bacteria attack this barrier with extracellular virulence factors, such as cell wall degrading enzymes, and bypass it by the secretion of cell wall-permeable toxins 5 . However, perhaps the most effective virulence strategy, and one shared with animal bacterial pathogens, is to breach the wall by use of the type III s...

show abstract

Section: Bacterial Suppression Of Hr-based Pcdsupporting

confidence: 91%

Bacterial elicitation and evasion of plant innate immunity

Abramovitch

Anderson

Martin

2006

Nat Rev Mol Cell Biol

Self Cite

375

285

View full text Add to dashboard Cite

show abstract

“…phaseolicola, it can restore water-soaking ability to this pathogen ( Jackson et al 2002). Recently, the phenotype of a double-mutant Pst strain, lacking both AvrPto and AvrPtoB, was generated (Lin and Martin 2005). This strain shows an even slower growth rate in susceptible hosts than either of the single mutant Pst strains, indicating that AvrPto and AvrPtoB contribute additively to virulence activity of Pst.…”

Section: Discussionmentioning

confidence: 99%

Natural Variation in the Pto Disease Resistance Gene Within Species of Wild Tomato (Lycopersicon). II. Population Genetics of Pto

Rose¹,

Michelmore²,

Langley

2007

Genetics

View full text Add to dashboard Cite

Disease resistance to the bacterial pathogen Pseudomonas syringae pv. tomato (Pst) in the host species Lycopersicon esculentum, the cultivated tomato, and the closely related L. pimpinellifolium is triggered by the physical interaction between the protein products of the host resistance (R) gene Pto and the pathogen avirulence genes AvrPto and AvrPtoB. Sequence variation at the Pto locus was surveyed in natural populations of seven species of Lycopersicon to test hypotheses of host-parasite coevolution and functional adaptation of the Pto gene. Pto shows significantly higher nonsynonymous polymorphism than 14 other non-R-gene loci in the same samples of Lycopersicon species, while showing no difference in synonymous polymorphism, suggesting that the maintenance of amino acid polymorphism at this locus is mediated by pathogen selection. Also, a larger proportion of ancestral variation is maintained at Pto as compared to these non-R-gene loci. The frequency spectrum of amino acid polymorphisms known to negatively affect Pto function is skewed toward low frequency compared to amino acid polymorphisms that do not affect function or silent polymorphisms. Therefore, the evolution of Pto appears to be influenced by a mixture of both purifying and balancing selection.

show abstract

“…After Rs10703 inoculation, plants were return to the greenhouse. Disease assessment and estimation of pathogen growth in planta were carried out as described (Lin and Martin, 2005;Saile et al, 1997). Five days after inoculation, DC 3000 and speck numbers were estimated for five representative areas (2 × 2 cm 2 ) which showed discrete lesions.…”

Section: Plants and Pathogen Challengementioning

confidence: 99%

Priming by Rhizobacterium Protects Tomato Plants from Biotrophic and Necrotrophic Pathogen Infections through Multiple Defense Mechanisms

Ahn

Lee

Kim

et al. 2011

Molecules and Cells

View full text Add to dashboard Cite

A selected strain of rhizobacterium, Pseudomonas putida strain LSW17S (LSW17S), protects tomato plants (Lycopersicon esculentum L. cv. Seokwang) from bacterial speck by biotrophic Pseudomonas syringae pv. tomato strain DC3000 (DC3000) and bacterial wilt by necrotrophic Ralstonia solanacearum KACC 10703 (Rs10703). To investigate defense mechanisms induced by LSW17S in tomato plants, transcription patterns of pathogenesis-related (PR) genes and H 2 O 2 production were analyzed in plants treated with LSW17S and subsequent pathogen inoculation. LSW17S alone did not induce transcriptions of employed PR genes in leaves and roots. DC3000 challenge following LSW17S triggered rapid transcriptions of PR genes and H 2 O 2 production in leaves and roots. Catalase infiltration with DC3000 attenuated defense-related responses and resistance against DC3000 infection. Despite depriving H 2 O 2 production and PR1b transcription by the same treatment, resistance against Rs10703 infection was not deterred significantly. H 2 O 2 is indispensable for defense signaling and/or mechanisms primed by LSW17S and inhibition of bacterial speck, however, it is not involved in resistance against bacterial wilt.

show abstract

An avrPto/avrPtoB Mutant of Pseudomonas syringae pv. tomato DC3000 Does Not Elicit Pto-Mediated Resistance and Is Less Virulent on Tomato

Cited by 134 publications

References 50 publications

Bacterial elicitation and evasion of plant innate immunity

Bacterial elicitation and evasion of plant innate immunity

Natural Variation in the Pto Disease Resistance Gene Within Species of Wild Tomato (Lycopersicon). II. Population Genetics of Pto

Priming by Rhizobacterium Protects Tomato Plants from Biotrophic and Necrotrophic Pathogen Infections through Multiple Defense Mechanisms

Contact Info

Product

Resources

About