scholarly journals Specific In Planta Recognition of Two GKLR Proteins of the Downy Mildew Bremia lactucae Revealed in a Large Effector Screen in Lettuce

2013 ◽  
Vol 26 (11) ◽  
pp. 1259-1270 ◽  
Author(s):  
Joost H. M. Stassen ◽  
Erik den Boer ◽  
Pim W. J. Vergeer ◽  
Annemiek Andel ◽  
Ursula Ellendorff ◽  
...  
Keyword(s):  
Immune Responses ◽  
Downy Mildew ◽  
Hypersensitive Response ◽  
Effector Proteins ◽  
Chromosome 9 ◽  
Downy Mildew Resistance ◽  
Chromosome 2 ◽  
Bremia Lactucae ◽  
In Planta ◽  
Effector Triggered Immunity

Breeding lettuce (Lactuca sativa) for resistance to the downy mildew pathogen Bremia lactucae is mainly achieved by introgression of dominant downy mildew resistance (Dm) genes. New Bremia races quickly render Dm genes ineffective, possibly by mutation of recognized host-translocated effectors or by suppression of effector-triggered immunity. We have previously identified 34 potential RXLR(-like) effector proteins of B. lactucae that were here tested for specific recognition within a collection of 129 B. lactucae-resistant Lactuca lines. Two effectors triggered a hypersensitive response: BLG01 in 52 lines, predominantly L. saligna, and BLG03 in two L. sativa lines containing Dm2 resistance. The N-terminal sequences of BLG01 and BLG03, containing the signal peptide and GKLR variant of the RXLR translocation motif, are not required for in planta recognition but function in effector delivery. The locus responsible for BLG01 recognition maps to the bottom of lettuce chromosome 9, whereas recognition of BLG03 maps in the RGC2 cluster on chromosome 2. Lactuca lines that recognize the BLG effectors are not resistant to Bremia isolate Bl:24 that expresses both BLG genes, suggesting that Bl:24 can suppress the triggered immune responses. In contrast, lettuce segregants displaying Dm2-mediated resistance to Bremia isolate Bl:5 are responsive to BLG03, suggesting that BLG03 is a candidate Avr2 protein.

scholarly journals Mutants of downy mildew resistance in Lactuca sativa (lettuce).

Genetics ◽  
1994 ◽  
Vol 137 (3) ◽  
pp. 867-874
Author(s):  
P A Okubara ◽  
P A Anderson ◽  
O E Ochoa ◽  
R W Michelmore
Keyword(s):  
Molecular Marker ◽  
Downy Mildew ◽  
Genomic Dna ◽  
Spontaneous Mutation ◽  
Multigene Families ◽  
Downy Mildew Resistance ◽  
Bremia Lactucae ◽  
Wild Type ◽  
Mildew Resistance ◽  
Recessive Mutations

Abstract As part of our investigation of disease resistance in lettuce, we generated mutants that have lost resistance to Bremia lactucae, the casual fungus of downy mildew. Using a rapid and reliable screen, we identified 16 distinct mutants of Latuca sativa that have lost activity of one of four different downy mildew resistance genes (Dm). In all mutants, only a single Dm specificity was affected. Genetic analysis indicated that the lesions segregated as single, recessive mutations at the Dm loci. Dm3 was inactivated in nine of the mutants. One of five Dm 1 mutants was selected from a population of untreated seeds and therefore carried a spontaneous mutation. All other Dm1, Dm3, Dm5/8 and Dm7 mutants were derived from gamma- or fast neutron-irradiated seed. In two separate Dm 1 mutants and in each of the eight Dm3 mutants analyzed, at least one closely linked molecular marker was absent. Also, high molecular weight genomic DNA fragments that hybridized to a tightly linked molecular marker in wild type were either missing entirely or were truncated in two of the Dm3 mutants, providing additional evidence that deletions had occurred in these mutants. Absence of mutations at loci epistatic to the Dm genes suggested that such loci were either members of multigene families, were critical for plant survival, or encoded components of duplicated pathways for resistance; alternatively, the genes determining downy mildew resistance might be limited to the Dm loci.

scholarly journals Host interactors of effector proteins of the lettuce downy mildew Bremia lactucae obtained by yeast two-hybrid screening

PLoS ONE ◽  
2020 ◽  
Vol 15 (5) ◽  
pp. e0226540 ◽  
Author(s):  
Alexandra J. E. Pelgrom ◽  
Claudia-Nicole Meisrimler ◽  
Joyce Elberse ◽  
Thijs Koorman ◽  
Mike Boxem ◽  
...  
Keyword(s):  
Downy Mildew ◽  
Effector Proteins ◽  
Bremia Lactucae ◽  
Yeast Two Hybrid ◽  
Lettuce Downy Mildew ◽  
Two Hybrid ◽  
Hybrid Screening

scholarly journals Host targets of effectors of the lettuce downy mildew Bremia lactucae from cDNA-based yeast two-hybrid screening

2019 ◽  
Author(s):  
Alexandra J.E. Pelgrom ◽  
Claudia-Nicole Meisrimler ◽  
Joyce Elberse ◽  
Thijs Koorman ◽  
Mike Boxem ◽  
...  
Keyword(s):  
Downy Mildew ◽  
Pathogenic Bacteria ◽  
Plant Pathogens ◽  
Molecular Mechanisms ◽  
Effector Proteins ◽  
Bremia Lactucae ◽  
Yeast Two Hybrid ◽  
Target Proteins ◽  
Successful Infection ◽  
Two Hybrid

AbstractPlant pathogenic bacteria, fungi and oomycetes secrete effector proteins to manipulate host cell processes to establish a successful infection. Over the last decade the genomes and transcriptomes of many agriculturally important plant pathogens have been sequenced and vast candidate effector repertoires were identified using bioinformatic analyses. Elucidating the contribution of individual effectors to pathogenicity is the next major hurdle. To advance our understanding of the molecular mechanisms underlying lettuce susceptibility to the downy mildew Bremia lactucae, we mapped a network of physical interactions between B. lactucae effectors and lettuce target proteins. Using a lettuce cDNA library-based yeast-two-hybrid system, 61 protein-protein interactions were identified, involving 21 B. lactucae effectors and 46 unique lettuce proteins. The top ten targets based on the number of independent colonies identified in the Y2H and two targets that belong to gene families involved in plant immunity, were further characterized. We determined the subcellular localization of the fluorescently tagged target proteins and their interacting effectors. Importantly, relocalization of effectors or targets to the nucleus was observed for four effector-target pairs upon their co-expression, supporting their interaction in planta.

scholarly journals A Pseudomonas syringae pv. tomato avrE1/hopM1 Mutant Is Severely Reduced in Growth and Lesion Formation in Tomato

2006 ◽  
Vol 19 (2) ◽  
pp. 99-111 ◽  
Author(s):  
Jorge L. Badel ◽  
Rena Shimizu ◽  
Hye-Sook Oh ◽  
Alan Collmer
Keyword(s):  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Plant Cells ◽  
Effector Proteins ◽  
35S Promoter ◽  
In Planta ◽  
Lesion Formation ◽  
Effector Genes ◽  
Combined Action ◽  
Different Levels

The model plant pathogen Pseudomonas syringae pv. tomato DC3000 grows and produces necrotic lesions in the leaves of its host, tomato. Both abilities are dependent upon the hypersensitive response and pathogenicity (Hrp) type III secretion system (TTSS), which translocates multiple effector proteins into plant cells. A previously constructed DC3000 mutant with a 9.3-kb deletion in the Hrp pathogenicity island conserved effector locus (CEL) was strongly reduced in growth and lesion formation in tomato leaves. The ΔCEL mutation affects three putative or known effector genes: avrE1, hopM1, and hopAA1-1. Comparison of genomic sequences of DC3000, P. syringae pv. phaseolicola 1448A, and P. syringae pv. syringae B728a revealed that these are the only effector genes present in the CEL of all three strains. AvrE1 was shown to carry functional TTSS translocation signals based on the performance of a fusion of the first 315 amino acids of AvrE1 to the Cya translocation reporter. A DC3000 ΔavrE1 mutant was reduced in its ability to produce lesions but not in its ability to grow in host tomato leaves. AvrE1 expressed from the 35S promoter elicited cell death in nonhost Nicotiana tabacum leaves and host tomato leaves in Agrobacterium-mediated transient expression experiments. Mutations involving combinations of avrE1, hopM1, and hopAA1-1 revealed that deletion of both avrE1 and hopM1 reproduced the strongly reduced growth and lesion phenotype of the ΔCEL mutant. Furthermore, quantitative assays involving different levels of inoculum and electrolyte leakage revealed that the avrE1/hopM1 and ΔCEL mutants both were partially impaired in their ability to elicit the hypersensitive response in nonhost N. benthamiana leaves. However, the avrE1/hopM1 mutant was not impaired in its ability to deliver AvrPto1(1–100)-Cya to nonhost N. benthamiana or host tomato leaves during the first 9 h after inoculation. These data suggest that AvrE1 acts within plant cells and promotes lesion formation and that the combined action of AvrE1 and HopM1 is particularly important in promoting bacterial growth in planta.

scholarly journals Receptors in the induction of the plant innate immunity

2021 ◽  
Author(s):  
Tian-Ying Yu ◽  
Meng-Kun Sun ◽  
Li-Kun Liang
Keyword(s):  
Immune Responses ◽  
Innate Immune System ◽  
Effector Proteins ◽  
Innate Immune ◽  
Leucine Rich Repeat ◽  
Nucleotide Binding Domain ◽  
Effector Triggered Immunity ◽  
Growth Development ◽  
Immune Pathway ◽  
Molecular Patterns

Plants adjust amplitude and duration of immune responses via different strategies to maintain growth, development and resistance to pathogens. Pathogen-associated molecular patterns (PAMPs)-triggered immunity (PTI) and effector-triggered immunity (ETI) play vital roles. PRRs (pattern recognition receptors), comprising a large number of receptor-like protein kinases (RLKs) and receptor-like proteins (RLPs), recognize related ligands and trigger immunity. PTI is the first layer of the innate immune system, and it recognizes PAMPs at plasma membrane to prevent infection. However, pathogens exploit effector proteins to bypass or directly inhibit the PTI immune pathway. Consistently, plants have evolved intracellular nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins to detect pathogenic effectors and trigger a hypersensitive response to activate ETI. PTI and ETI work together to protect plants from infection of virus and other pathogens. Diverse receptors and the corresponding ligands, especially several pairs of well-studied receptors and ligands in PTI immunity, are reviewed to illustrate the dynamic process of PTI response here.

scholarly journals Effector loss drives adaptation of Pseudomonas syringae pv. actinidiae to Actinidia arguta

2021 ◽  
Author(s):  
Lauren M Hemara ◽  
Jay Jayaraman ◽  
Paul Sutherland ◽  
Mirco Montefiori ◽  
Saadiah Arshed ◽  
...  
Keyword(s):  
Pseudomonas Syringae ◽  
Hypersensitive Response ◽  
Durable Resistance ◽  
Host Recognition ◽  
Ion Leakage ◽  
In Planta ◽  
Resistance Response ◽  
Bacterial Pathogenicity ◽  
Effector Triggered Immunity ◽  
Species Specific

A pandemic isolate of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has devastated kiwifruit orchards growing cultivars of Actinidia chinensis. In contrast, A. arguta (kiwiberry) is resistant to Psa3. This resistance is mediated via effector-triggered immunity, as demonstrated by induction of the hypersensitive response in infected A. arguta leaves, observed by microscopy and quantified by ion-leakage assays. Isolates of Psa3 that cause disease in A. arguta have been isolated and analyzed, revealing a 49 kb deletion in the exchangeable effector locus (EEL). This natural EEL-mutant isolate and strains with synthetic knockouts of the EEL were more virulent in A. arguta plantlets than wild-type Psa3. Screening of a complete library of Psa3 effector knockout strains identified increased growth in planta for knockouts of four effectors — AvrRpm1a, HopF1c, HopZ5a, and the EEL effector HopAW1a — suggesting a resistance response in A. arguta. Hypersensitive response (HR) assays indicate that three of these effectors trigger a host species-specific HR. A Psa3 strain with all four effectors knocked out escaped host recognition, but a cumulative increase in bacterial pathogenicity and virulence was not observed. These avirulence effectors can be used in turn to identify the first cognate resistance genes in Actinidia for breeding durable resistance into future kiwifruit cultivars.

scholarly journals Perception of structurally distinct effectors by the integrated WRKY domain of a plant immune receptor.

2021 ◽  
Author(s):  
Nitika Mukhi ◽  
Hannah Brown ◽  
Danylo Gorenkin ◽  
Pingtao Ding ◽  
Adam R Bentham ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Immune Responses ◽  
Pseudomonas Syringae ◽  
Effector Proteins ◽  
Dna Binding Domain ◽  
Binding Affinities ◽  
Wrky Domain ◽  
In Planta ◽  
Integrated Domains

Plants use intracellular immune receptors (NLRs) to detect pathogen-derived effector proteins. The Arabidopsis NLR pair RRS1-R/RPS4 confers disease resistance to different bacterial pathogens by perceiving structurally distinct effectors AvrRps4 from Pseudomonas syringae pv. pisi and PopP2 from Ralstonia solanacearum via an integrated WRKY domain in RRS1-R. How the WRKY domain of RRS1 (RRS1WRKY) perceives distinct classes of effector to initiate an immune response is unknown. We report here the crystal structure of the in planta processed C-terminal domain of AvrRps4 (AvrRps4C) in complex with RRS1WRKY. Perception of AvrRps4C by RRS1WRKY is mediated by the β2-β3 segment of RRS1WRKY that binds an electronegative patch on the surface of AvrRps4C. Structure-based mutations that disrupt AvrRps4C/RRS1WRKY interactions in vitro compromise RRS1/RPS4-dependent immune responses. We also show that AvrRps4C can associate with the WRKY domain of the related but distinct RRS1B/RPS4B NLR pair, and the DNA binding domain of AtWRKY41, with similar binding affinities. This work demonstrates how integrated domains in plant NLRs can directly bind structurally distinct effectors to initiate immunity.

scholarly journals Albugo candida (white rust) suppresses resistance to downy mildew pathogens in Arabidopsis thaliana

2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 474-476 ◽  
Author(s):  
A.J. Cooper ◽  
A. Woods-Tör ◽  
E.B. Holub
Keyword(s):  
Arabidopsis Thaliana ◽  
Downy Mildew ◽  
Rust Resistance ◽  
Downy Mildew Resistance ◽  
Bremia Lactucae ◽  
Structural Class ◽  
Albugo Candida ◽  
White Rust ◽  
Downy Mildews ◽  
Hyaloperonospora Parasitica

Arabidopsis thaliana accessions were inoculated with incompatible isolates of downy mildews, following pre-inoculation with compatible Albugo candida. Three isolates of Hyaloperonospora parasitica subsp. A. thaliana, an isolate of H. parasitica subsp. Brassica oleracea and one Bremia lactucae (lettuce) isolate were included. All downy mildews sporulated on A. thaliana, suggesting A. candida suppresses broad-spectrum downy mildew resistance. The white rust resistance gene, RAC5, is being investigated. The resistance phenotype associated with RAC5 seems not to involve a hypersensitive response. RAC5 has been mapped telomeric of nga106 on chromosome 5, in a region lacking NB-LRR genes, the most common structural class of resistance genes known in A. thaliana.

Genetic analysis of downy mildew resistance and identification of molecular markers linked to resistance gene Ppa207 on chromosome 2 in cauliflower

Euphytica ◽  
2020 ◽  
Vol 216 (11) ◽  
Author(s):  
Partha Saha ◽  
Chandrika Ghoshal ◽  
Soham Ray ◽  
Namita Das Saha ◽  
Mohita Srivastava ◽  
...  
Keyword(s):  
Molecular Markers ◽  
Genetic Analysis ◽  
Downy Mildew ◽  
Resistance Gene ◽  
Downy Mildew Resistance ◽  
Chromosome 2 ◽  
Mildew Resistance

scholarly journals Mechanisms of Effector-Mediated Immunity Revealed by the Accidental Human Pathogen Legionella pneumophila

2021 ◽  
Vol 10 ◽  
Author(s):  
Tshegofatso Ngwaga ◽  
Deepika Chauhan ◽  
Stephanie R. Shames
Keyword(s):  
Immune Responses ◽  
Legionella Pneumophila ◽  
Bacterial Pathogens ◽  
Effector Proteins ◽  
Host Cells ◽  
Human Pathogen ◽  
Future Prospects ◽  
Gram Negative ◽  
Rapid Spread ◽  
Effector Triggered Immunity

Many Gram-negative bacterial pathogens employ translocated virulence factors, termed effector proteins, to facilitate their parasitism of host cells and evade host anti-microbial defenses. However, eukaryotes have evolved to detect effector-mediated virulence strategies through a phenomenon termed effector-triggered immunity (ETI). Although ETI was discovered in plants, a growing body of literature demonstrates that metazoans also utilize effector-mediated immunity to detect and clear bacterial pathogens. This mini review is focused on mechanisms of effector-mediated immune responses by the accidental human pathogen Legionella pneumophila. We highlight recent advancements in the field and discuss the future prospects of harnessing effectors for the development of novel therapeutics, a critical need due to the prevalence and rapid spread of antibiotic resistance.

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