Irish Potato Famine

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 936 Experts worldwide ranked by ideXlab platform

Sophien Kamoun - One of the best experts on this subject based on the ideXlab platform.

  • regressive evolution of an effector following a host jump in the Irish Potato Famine pathogen lineage
    bioRxiv, 2021
    Co-Authors: Tolga O. Bozkurt, Abbas Maqbool, Yasin F Dagdas, Erin K Zess, Esme Peers, Mark J Banfield, Sophien Kamoun
    Abstract:

    In order to infect a new host species, the pathogen must evolve to enhance infection and transmission in the novel environment. Although we often think of evolution as a process of accumulation, it is also a process of loss. Here, we document an example of regressive evolution in the Irish Potato Famine pathogen (Phytophthora infestans) lineage, providing evidence that a key sequence motif in the effector PexRD54 has degenerated following a host jump. We began by looking at PexRD54 and PexRD54-like sequences from across Phytophthora species. We found that PexRD54 emerged in the common ancestor of Phytophthora clade 1b and 1c species, and further sequence analysis showed that a key functional motif, the C-terminal ATG8-interacting motif (AIM), was also acquired at this point in the lineage. A closer analysis showed that the P. mirabilis PexRD54 (PmPexRD54) AIM appeared unusual, the otherwise-conserved central residue mutated from a glutamate to a lysine. We aimed to determine whether this PmPexRD54 AIM polymorphism represented an adaptation to the Mirabilis jalapa host environment. We began by characterizing the M. jalapa ATG8 family, finding that they have a unique evolutionary history compared to previously characterized ATG8s. Then, using co-immunoprecipitation and isothermal titration calorimetry assays, we showed that both full-length PmPexRD54 and the PmPexRD54 AIM peptide bind very weakly to the M. jalapa ATG8s. Through a combination of binding assays and structural modelling, we showed that the identity of the residue at the position of the PmPexRD54 AIM polymorphism can underpin high-affinity binding to plant ATG8s. Finally, we conclude that the functionality of the PexRD54 AIM was lost in the P. mirabilis lineage, perhaps owing to as-yet-unknown pressure on this effector in the new host environment. Author SummaryPathogens evolve in concert with their hosts. When a pathogen begins to infect a new host species, known as a "host jump," the pathogen must evolve to enhance infection and transmission. These evolutionary processes can involve both the gain and loss of genes, as well as dynamic changes in protein function. Here, we describe an example of a pathogen protein that lost a key functional domain following a host jump, a salient example of "regressive evolution." Specifically, we show that an effector protein from the plant pathogen Phytopthora mirabilis, a host-specific lineage closely related to the Irish Potato Famine pathogen Phytopthora infestans, has a derived amino acid polymorphism that results in a loss of interaction with certain host machinery.

  • prereview of biorxiv article genome wide increased copy number is associated with emergence of super fit clones of the Irish Potato Famine pathogen phytophthora infestans
    Authorea Preprints, 2019
    Co-Authors: Sophien Kamoun
    Abstract:

    This is a review of Knaus et al. bioRxiv doi: https://doi.org/10.1101/633701 posted on May 16, 2019. In this paper, the authors studied variations in ploidy in a wide range of isolates of the Potato blight pathogen Phytophthora infestans.

  • The malarial host-targeting signal is conserved in the Irish Potato Famine pathogen.
    2018
    Co-Authors: Souvik Bhattacharjee, Sophien Kamoun, Konstantinos Liolios, Joe Win, Thirumaladevi Kanneganti, Natalia Hiller, Carolyn Young, Kasturi Haldar
    Abstract:

    Animal and plant eukaryotic pathogens, such as the human malaria parasite Plasmodium falciparum and the Potato late blight agent Phytophthora infestans, are widely divergent eukaryotic microbes. Yet they both produce secretory virulence and pathogenic proteins that alter host cell functions. In P. falciparum, export of parasite proteins to the host erythrocyte is mediated by leader sequences shown to contain a host-targeting (HT) motif centered on an RxLx (E, D, or Q) core: this motif appears to signify a major pathogenic export pathway with hundreds of putative effectors. Here we show that a secretory protein of P. infestans, which is perceived by plant disease resistance proteins and induces hypersensitive plant cell death, contains a leader sequence that is equivalent to the Plasmodium HT-leader in its ability to export fusion of green fluorescent protein (GFP) from the P. falciparum parasite to the host erythrocyte. This export is dependent on an RxLR sequence conserved in P. infestans leaders, as well as in leaders of all ten secretory oomycete proteins shown to function inside plant cells. The RxLR motif is also detected in hundreds of secretory proteins of P. infestans, Phytophthora sojae, and Phytophthora ramorum and has high value in predicting host-targeted leaders. A consensus motif further reveals E/D residues enriched within approximately 25 amino acids downstream of the RxLR, which are also needed for export. Together the data suggest that in these plant pathogenic oomycetes, a consensus HT motif may reside in an extended sequence of approximately 25-30 amino acids, rather than in a short linear sequence. Evidence is presented that although the consensus is much shorter in P. falciparum, information sufficient for vacuolar export is contained in a region of approximately 30 amino acids, which includes sequences flanking the HT core. Finally, positional conservation between Phytophthora RxLR and P. falciparum RxLx (E, D, Q) is consistent with the idea that the context of their presentation is constrained. These studies provide the first evidence to our knowledge that eukaryotic microbes share equivalent pathogenic HT signals and thus conserved mechanisms to access host cells across plant and animal kingdoms that may present unique targets for prophylaxis across divergent pathogens.

  • gene expression polymorphism underpins evasion of host immunity in an asexual lineage of the Irish Potato Famine pathogen
    bioRxiv, 2017
    Co-Authors: Marina Pais, Ricardo Oliva, Kentaro Yoshida, Liliana M Cano, Artemis Giannakopoulou, Mathieu A Pel, Kamil Witek, Hannele Lindqvistkreuze, Vivianne G A A Vleeshouwers, Sophien Kamoun
    Abstract:

    Outbreaks caused by asexual lineages of fungal and oomycete pathogens are an expanding threat to crops, wild animals and natural ecosystems (Fisher et al. 2012, Kupferschmidt 2012). However, the mechanisms underlying genome evolution and phenotypic plasticity in asexual eukaryotic microbes remain poorly understood (Seidl and Thomma 2014). Ever since the 19th century Irish Famine, the oomycete Phytophthora infestans has caused recurrent outbreaks on Potato and tomato crops that have been primarily caused by the successive rise and migration of pandemic asexual lineages (Cooke et al. 2012, Yoshida et al. 2013, Yoshida et al. 2014). Here, we reveal patterns of genomic and gene expression variation within a P. infestans asexual lineage by compared sibling strains belonging to the South American EC-1 clone that has dominated Andean populations since the 1990s (Forbes et al. 1997, Oyarzun et al. 1998, Delgado et al. 2013, Yoshida et al. 2013, Yoshida et al. 2014). We detected numerous examples of structural variation, nucleotide polymorphisms and gene conversion within the EC-1 clone. Remarkably, 17 genes are not expressed in one of the two EC-1 isolates despite apparent absence of sequence polymorphisms. Among these, silencing of an effector gene was associated with evasion of disease resistance conferred by a Potato immune receptor. These results highlight the exceptional genetic and phenotypic plasticity that underpins host adaptation in a pandemic clonal lineage of a eukaryotic plant pathogen.

  • structural basis of host autophagy related protein 8 atg8 binding by the Irish Potato Famine pathogen effector protein pexrd54
    Journal of Biological Chemistry, 2016
    Co-Authors: Abbas Maqbool, Tolga O. Bozkurt, Richard K Hughes, Yasin F Dagdas, Nicholas Tregidgo, Erin K Zess, Khaoula Belhaj, Adam Round, Sophien Kamoun
    Abstract:

    Filamentous plant pathogens deliver effector proteins to host cells to promote infection. The Phytophthora infestans RXLR-type effector PexRD54 binds Potato ATG8 via its ATG8 family-interacting motif (AIM) and perturbs host-selective autophagy. However, the structural basis of this interaction remains unknown. Here, we define the crystal structure of PexRD54, which includes a modular architecture, including five tandem repeat domains, with the AIM sequence presented at the disordered C terminus. To determine the interface between PexRD54 and ATG8, we solved the crystal structure of Potato ATG8CL in complex with a peptide comprising the effector's AIM sequence, and we established a model of the full-length PexRD54-ATG8CL complex using small angle x-ray scattering. Structure-informed deletion of the PexRD54 tandem domains reveals retention of ATG8CL binding in vitro and in planta. This study offers new insights into structure/function relationships of oomycete RXLR effectors and how these proteins engage with host cell targets to promote disease.

Niklaus J Grunwald - One of the best experts on this subject based on the ideXlab platform.

  • genome wide increased copy number is associated with emergence of dominant clones of the Irish Potato Famine pathogen phytophthora infestans
    Mbio, 2020
    Co-Authors: Brian J. Knaus, Javier F. Tabima, Howard S. Judelson, Shankar K Shakya, Niklaus J Grunwald
    Abstract:

    The plant pathogen that caused the Irish Potato Famine, Phytophthora infestans, continues to reemerge globally. These modern epidemics are caused by clonally reproducing lineages. In contrast, a sexual mode of reproduction is observed at its center of origin in Mexico. We conducted a comparative genomic analysis of 47 high-coverage genomes to infer changes in genic copy number. We included samples from sexual populations at the center of origin as well as several dominant clonal lineages sampled worldwide. We conclude that sexual populations at the center of origin are diploid, as was the lineage that caused the Famine, while modern clonal lineages showed increased copy number (3×). Copy number variation (CNV) was found genome-wide and did not to adhere to the two-speed genome hypothesis. Although previously reported, tetraploidy was not found in any of the genomes evaluated. We propose a model of dominant clone emergence supported by the epidemiological record (e.g., EU_13_A2, US-11, US-23) whereby a higher copy number provides fitness, leading to replacement of prior clonal lineages.IMPORTANCE The plant pathogen implicated in the Irish Potato Famine, Phytophthora infestans, continues to reemerge globally. Understanding changes in the genome during emergence can provide insights useful for managing this pathogen. Previous work has relied on studying individuals from the United States, South America, Europe, and China reporting that these can occur as diploids, triploids, or tetraploids and are clonal. We studied variation in sexual populations at the pathogen's center of origin, in Mexico, where it has been reported to reproduce sexually as well as within clonally reproducing, dominant clones from the United States and Europe. Our results newly show that sexual populations at the center of origin are diploid, whereas populations elsewhere are more variable and show genome-wide variation in gene copy number. We propose a model of evolution whereby new pathogen clones emerge predominantly by increasing the gene copy number genome-wide.

  • Genome-Wide Increased Copy Number is Associated with Emergence of Dominant Clones of the Irish Potato Famine Pathogen Phytophthora infestans
    'American Society for Microbiology', 2020
    Co-Authors: Brian J. Knaus, Javier F. Tabima, Howard S. Judelson, Shankar K Shakya, Niklaus J Grunwald
    Abstract:

    The plant pathogen implicated in the Irish Potato Famine, Phytophthora infestans, continues to reemerge globally. Understanding changes in the genome during emergence can provide insights useful for managing this pathogen. Previous work has relied on studying individuals from the United States, South America, Europe, and China reporting that these can occur as diploids, triploids, or tetraploids and are clonal. We studied variation in sexual populations at the pathogen’s center of origin, in Mexico, where it has been reported to reproduce sexually as well as within clonally reproducing, dominant clones from the United States and Europe. Our results newly show that sexual populations at the center of origin are diploid, whereas populations elsewhere are more variable and show genome-wide variation in gene copy number. We propose a model of evolution whereby new pathogen clones emerge predominantly by increasing the gene copy number genome-wide.The plant pathogen that caused the Irish Potato Famine, Phytophthora infestans, continues to reemerge globally. These modern epidemics are caused by clonally reproducing lineages. In contrast, a sexual mode of reproduction is observed at its center of origin in Mexico. We conducted a comparative genomic analysis of 47 high-coverage genomes to infer changes in genic copy number. We included samples from sexual populations at the center of origin as well as several dominant clonal lineages sampled worldwide. We conclude that sexual populations at the center of origin are diploid, as was the lineage that caused the Famine, while modern clonal lineages showed increased copy number (3×). Copy number variation (CNV) was found genome-wide and did not to adhere to the two-speed genome hypothesis. Although previously reported, tetraploidy was not found in any of the genomes evaluated. We propose a model of dominant clone emergence supported by the epidemiological record (e.g., EU_13_A2, US-11, US-23) whereby a higher copy number provides fitness, leading to replacement of prior clonal lineages

  • Genome-wide increased copy number is associated with emergence of super-fit clones of the Irish Potato Famine pathogen Phytophthora infestans
    bioRxiv, 2019
    Co-Authors: Brian J. Knaus, Shankar Shakya, Javier F. Tabima, Howard S. Judelson, Niklaus J Grunwald
    Abstract:

    Abstract The plant pathogen that caused the Irish Potato Famine, Phytophthora infestans, continues to reemerge globally. These modern epidemics are caused by clonally reproducing lineages. In contrast, a sexual mode of reproduction is observed at its center of origin in Mexico. We conducted a comparative genomic analysis of 47 high coverage genomes to infer changes in genic copy number. We included samples from sexual populations at the center of origin as well as several dominant clonal lineages sampled worldwide. We conclude that sexual populations at the center of origin are diploid as was the lineage that caused the Famine, while modern clonal lineages showed increased copy number (3x). Copy number variation (CNV) was found genome-wide and did not to adhere to the two-speed genome hypothesis. Although previously reported, tetraploidy was not found in any of the genomes evaluated. We propose a model of super-fit clone emergence supported by the epidemiological record (e.g., EU_13_A2, US-11, US-23) whereby higher copy number provides fitness leading to replacement of prior clonal lineages.

  • five reasons to consider phytophthora infestans a reemerging pathogen
    Phytopathology, 2015
    Co-Authors: Paul R J Birch, Niklaus J Grunwald, Howard S. Judelson, Giovanna Danies, Kathryne L Everts, Amanda J Gevens, Beth K Gugino, Dennis A Johnson, Steven B Johnson, Margaret T Mcgrath
    Abstract:

    Phytophthora infestans has been a named pathogen for well over 150 years and yet it continues to “emerge”, with thousands of articles published each year on it and the late blight disease that it causes. This review explores five attributes of this oomycete pathogen that maintain this constant attention. First, the historical tragedy associated with this disease (Irish Potato Famine) causes many people to be fascinated with the pathogen. Current technology now enables investigators to answer some questions of historical significance. Second, the devastation caused by the pathogen continues to appear in surprising new locations or with surprising new intensity. Third, populations of P. infestans worldwide are in flux, with changes that have major implications to disease management. Fourth, the genomics revolution has enabled investigators to make tremendous progress in terms of understanding the molecular biology (especially the pathogenicity) of P. infestans. Fifth, there remain many compelling unanswered...

  • five reasons to consider phytophthora infestans a reemerging pathogen
    Phytopathology, 2015
    Co-Authors: William E. Fry, Niklaus J Grunwald, Howard S. Judelson, Paul R J Birch, Giovanna Danies, Kathryne L Everts, Amanda J Gevens, Beth K Gugino, Dennis A Johnson, Steven B Johnson
    Abstract:

    Phytophthora infestans has been a named pathogen for well over 150 years and yet it continues to "emerge", with thousands of articles published each year on it and the late blight disease that it causes. This review explores five attributes of this oomycete pathogen that maintain this constant attention. First, the historical tragedy associated with this disease (Irish Potato Famine) causes many people to be fascinated with the pathogen. Current technology now enables investigators to answer some questions of historical significance. Second, the devastation caused by the pathogen continues to appear in surprising new locations or with surprising new intensity. Third, populations of P. infestans worldwide are in flux, with changes that have major implications to disease management. Fourth, the genomics revolution has enabled investigators to make tremendous progress in terms of understanding the molecular biology (especially the pathogenicity) of P. infestans. Fifth, there remain many compelling unanswered questions.

Erica M Goss - One of the best experts on this subject based on the ideXlab platform.

  • the Irish Potato Famine pathogen phytophthora infestans originated in central mexico rather than the andes
    Proceedings of the National Academy of Sciences of the United States of America, 2014
    Co-Authors: Erica M Goss, Javier F. Tabima, Gregory A Forbes, D E L Cooke, Silvia Restrepo, V J Fieland, Martha Cardenas, Niklaus J Grunwald
    Abstract:

    Phytophthora infestans is a destructive plant pathogen best known for causing the disease that triggered the Irish Potato Famine and remains the most costly Potato pathogen to manage worldwide. Identification of P. infestan’s elusive center of origin is critical to understanding the mechanisms of repeated global emergence of this pathogen. There are two competing theories, placing the origin in either South America or in central Mexico, both of which are centers of diversity of Solanum host plants. To test these competing hypotheses, we conducted detailed phylogeographic and approximate Bayesian computation analyses, which are suitable approaches to unraveling complex demographic histories. Our analyses used microsatellite markers and sequences of four nuclear genes sampled from populations in the Andes, Mexico, and elsewhere. To infer the ancestral state, we included the closest known relatives Phytophthora phaseoli, Phytophthora mirabilis, and Phytophthora ipomoeae, as well as the interspecific hybrid Phytophthora andina. We did not find support for an Andean origin of P. infestans; rather, the sequence data suggest a Mexican origin. Our findings support the hypothesis that populations found in the Andes are descendants of the Mexican populations and reconcile previous findings of ancestral variation in the Andes. Although centers of origin are well documented as centers of evolution and diversity for numerous crop plants, the number of plant pathogens with a known geographic origin are limited. This work has important implications for our understanding of the coevolution of hosts and pathogens, as well as the harnessing of plant disease resistance to manage late blight.

  • genome analyses of an aggressive and invasive lineage of the Irish Potato Famine pathogen
    PLOS Pathogens, 2012
    Co-Authors: D E L Cooke, Liliana M Cano, Sylvain Raffaele, Richard A Farrer, R A Bain, L R Cooke, Graham J Etherington, Kenneth L Deahl, Eleanor M Gilroy, Erica M Goss
    Abstract:

    Pest and pathogen losses jeopardise global food security and ever since the 19 th century Irish Famine, Potato late blight has exemplified this threat. The causal oomycete pathogen, Phytophthora infestans, undergoes major population shifts in agricultural systems via the successive emergence and migration of asexual lineages. The phenotypic and genotypic bases of these selective sweeps are largely unknown but management strategies need to adapt to reflect the changing pathogen population. Here, we used molecular markers to document the emergence of a lineage, termed 13_A2, in the European P. infestans population, and its rapid displacement of other lineages to exceed 75% of the pathogen population across Great Britain in less than three years. We show that isolates of the 13_A2 lineage are among the most aggressive on cultivated Potatoes, outcompete other aggressive lineages in the field, and overcome previously effective forms of plant host resistance. Genome analyses of a 13_A2 isolate revealed extensive genetic and expression polymorphisms particularly in effector genes. Copy number variations, gene gains and losses, amino-acid replacements and changes in expression patterns of disease effector genes within the 13_A2 isolate likely contribute to enhanced virulence and aggressiveness to drive this population displacement. Importantly, 13_A2 isolates carry intact and in planta induced Avrblb1, Avrblb2 and Avrvnt1 effector genes that trigger resistance in Potato lines carrying the corresponding R immune receptor genes Rpi-blb1, Rpi-blb2, and Rpi-vnt1.1. These findings point towards a strategy for deploying genetic resistance to mitigate the impact of the 13_A2 lineage and illustrate how pathogen population monitoring, combined with genome analysis, informs the management of devastating disease epidemics.

  • the plant pathogen phytophthora andina emerged via hybridization of an unknown phytophthora species and the Irish Potato Famine pathogen p infestans
    PLOS ONE, 2011
    Co-Authors: Erica M Goss, Gregory A Forbes, Silvia Restrepo, Martha Cardenas, Kevin Myers, Niklaus J Grunwald
    Abstract:

    Emerging plant pathogens have largely been a consequence of the movement of pathogens to new geographic regions. Another documented mechanism for the emergence of plant pathogens is hybridization between individuals of different species or subspecies, which may allow rapid evolution and adaptation to new hosts or environments. Hybrid plant pathogens have traditionally been difficult to detect or confirm, but the increasing ease of cloning and sequencing PCR products now makes the identification of species that consistently have genes or alleles with phylogenetically divergent origins relatively straightforward. We investigated the genetic origin of Phytophthora andina, an increasingly common pathogen of Andean crops Solanum betaceum, S. muricatum, S. quitoense, and several wild Solanum spp. It has been hypothesized that P. andina is a hybrid between the Potato late blight pathogen P. infestans and another Phytophthora species. We tested this hypothesis by cloning four nuclear loci to obtain haplotypes and using these loci to infer the phylogenetic relationships of P. andina to P. infestans and other related species. Sequencing of cloned PCR products in every case revealed two distinct haplotypes for each locus in P. andina, such that each isolate had one allele derived from a P. infestans parent and a second divergent allele derived from an unknown species that is closely related but distinct from P. infestans, P. mirabilis, and P. ipomoeae. To the best of our knowledge, the unknown parent has not yet been collected. We also observed sequence polymorphism among P. andina isolates at three of the four loci, many of which segregate between previously described P. andina clonal lineages. These results provide strong support that P. andina emerged via hybridization between P. infestans and another unknown Phytophthora species also belonging to Phytophthora clade 1c.

  • the plant pathogen phytophthora andina emerged via hybridization of an unknown phytophthora species and the Irish Potato Famine pathogen p infestans
    PLOS ONE, 2011
    Co-Authors: Erica M Goss, Gregory A Forbes, W E Fry, Silvia Restrepo, Martha Cardenas, Kevin Myers, Niklaus J Grunwald
    Abstract:

    Emerging plant pathogens have largely been a consequence of the movement of pathogens to new geographic regions. Another documented mechanism for the emergence of plant pathogens is hybridization between individuals of different species or subspecies, which may allow rapid evolution and adaptation to new hosts or environments. Hybrid plant pathogens have traditionally been difficult to detect or confirm, but the increasing ease of cloning and sequencing PCR products now makes the identification of species that consistently have genes or alleles with phylogenetically divergent origins relatively straightforward. We investigated the genetic origin of Phytophthora andina, an increasingly common pathogen of Andean crops Solanum betaceum, S. muricatum, S. quitoense, and several wild Solanum spp. It has been hypothesized that P. andina is a hybrid between the Potato late blight pathogen P. infestans and another Phytophthora species. We tested this hypothesis by cloning four nuclear loci to obtain haplotypes and using these loci to infer the phylogenetic relationships of P. andina to P. infestans and other related species. Sequencing of cloned PCR products in every case revealed two distinct haplotypes for each locus in P. andina, such that each isolate had one allele derived from a P. infestans parent and a second divergent allele derived from an unknown species that is closely related but distinct from P. infestans, P. mirabilis, and P. ipomoeae. To the best of our knowledge, the unknown parent has not yet been collected. We also observed sequence polymorphism among P. andina isolates at three of the four loci, many of which segregate between previously described P. andina clonal lineages. These results provide strong support that P. andina emerged via hybridization between P. infestans and another unknown Phytophthora species also belonging to Phytophthora clade 1c.

Jan Sklenar - One of the best experts on this subject based on the ideXlab platform.

  • an effector of the Irish Potato Famine pathogen antagonizes a host autophagy cargo receptor
    eLife, 2016
    Co-Authors: Yasin F Dagdas, Abbas Maqbool, Richard K Hughes, Khaoula Belhaj, Pooja Pandey, Benjamin Petre, Nadra Tabassum, Angela Chaparrogarcia, Neftaly Cruzmireles, Jan Sklenar
    Abstract:

    Plants and other living organisms can survive stress and starvation by digesting and recycling parts of their own cells. This process is known as autophagy and it involves engulfing cellular material inside spherical structures called autophagosomes, before delivering it to sites in the cell where digestive enzymes can break the material down. A form of autophagy, known as selective autophagy, can specifically degrade toxic substances such as disease-causing microbes. Selective autophagy works through proteins called autophagy cargo receptors that define which molecules are targeted for degradation. However, it was not clear whether autophagy protects plants from infections, or how much disease-causing microbes interfere with this process for their own benefit. The microbe that causes late blight of Potatoes (called Phytophthora infestans) is infamous for triggering widespread Famines in Ireland in the 19th century. This disease-causing microbe continues to pose a serious threat to food security today, and parasitizes plant tissues by releasing proteins called effectors that enter the plant’s cells to subvert the plant’s physiology and counteract its defenses. Dagdas, Belhaj et al. now report that an effector from P. infestans, called PexRD54, can bind to autophagy-related protein from Potato, called ATG8CL, and stimulate the formation of autophagosomes. Further experiments revealed that the PexRD54 effector could outcompete a plant autophagy cargo receptor that would otherwise bind to ATG8CL. This plant cargo receptor contributes to the plant’s defences, and by preventing it from interacting with ATG8CL, PexRD54 makes the plant more susceptible to infection by P. infestans. These findings show that the PexRD54 effector has evolved to interact with an autophagy-related protein to counteract the plant’s defences. Dagdas, Belhaj et al. suggest that PexRD54 might do this by activating autophagy to selectively eliminate some of the molecules that the plant use to defend itself. Furthermore, P. infestans might also benefit from the nutrients that are released when cellular material is broken down via autophagy. Future work could test these two hypotheses and explore whether other effectors from disease-causing microbes work in a similar way.

  • An effector of the Irish Potato Famine pathogen antagonizes a host autophagy cargo receptor
    eLife, 2016
    Co-Authors: Yasin F Dagdas, Abbas Maqbool, Khaoula Belhaj, Angela Chaparro-garcia, Pooja Pandey, Benjamin Petre, Nadra Tabassum, Neftaly Cruz-mireles, Richard Hughes, Jan Sklenar
    Abstract:

    Plants use autophagy to safeguard against infectious diseases. However, how plant pathogens interfere with autophagy-related processes is unknown. Here, we show that PexRD54, an effector from the Irish Potato Famine pathogen Phytophthora infestans, binds host autophagy protein ATG8CL to stimulate autophagosome formation. PexRD54 depletes the autophagy cargo receptor Joka2 out of ATG8CL complexes and interferes with Joka2's positive effect on pathogen defense. Thus, a plant pathogen effector has evolved to antagonize a host autophagy cargo receptor to counteract host defenses.

  • phytophthora infestans rxlr wy effector avr3a associates with a dynamin related protein involved in endocytosis of a plant pattern recognition receptor
    bioRxiv, 2014
    Co-Authors: Angela Chaparrogarcia, Tolga O. Bozkurt, Jan Sklenar, Kentaro Yoshida, Sebastian Schornack, Alexandra M E Jones, Simon Schwizer, Jorunn I B Bos, Sophien Kamoun
    Abstract:

    Perception of pathogen associated molecular patterns (PAMPs) by cell surface localized pattern recognition receptors (PPRs), activates plant basal defense responses in a process known as PAMP/PRR–triggered immunity (PTI). In turn, pathogens deploy effector proteins that interfere with different steps in PTI signaling. However, our knowledge of PTI suppression by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous work revealed that BAK1/SERK3, a regulatory receptor of several PRRs, contributes to basal immunity against the Irish Potato Famine pathogen Phytophthora infestans. Moreover BAK1/SERK3 is required for the cell death induced by P. infestans elicitin INF1, a protein with characteristics of PAMPs. The P. infestans host-translocated RXLR-WY effector AVR3a is known to supress INF1-mediated defense by binding the E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and suppress INF1 cell death. Here we studied the extent to which AVR3a and its variants perturb additional BAK1/SERK3 dependent PTI responses using the plant PRR FLAGELLIN SENSING 2 (FLS2). We found that all tested variants of AVR3a, including AVR3aKI-Y147del, suppress early defense responses triggered by the bacterial flagellin-derived peptide flg22 and reduce internalization of activated FLS2 from the plasma membrane without disturbing its nonactivated localization. Consistent with this effect of AVR3a on FLS2 endocytosis, we discovered that AVR3a associates with the Dynamin-Related Protein DRP2, a plant GTPase implicated in receptor-mediated endocytosis. Interestingly, DRP2 is required for ligand-induced FLS2 internalization but does not affect internalization of the growth receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1). Furthermore, overexpression of DRP2 suppressed accumulation of reactive oxygen species triggered by PAMP treatment. We conclude that AVR3a associates with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis and signaling. AVR3a is a multifunctional effector that can suppress BAK1/SERK3 mediated immunity through at least two different pathways.

  • Effector specialization in a lineage of the Irish Potato Famine pathogen
    Science, 2014
    Co-Authors: Suomeng Dong, Tolga O. Bozkurt, Ricardo Oliva, Remco Stam, Liliana M Cano, Jan Sklenar, Kentaro Yoshida, Jing Song, Zhenyu Liu, Miaoying Tian
    Abstract:

    Accelerated gene evolution is a hallmark of pathogen adaptation following a host jump. Here, we describe the biochemical basis of adaptation and specialization of a plant pathogen effector after its colonization of a new host. Orthologous protease inhibitor effectors from the Irish Potato Famine pathogen, Phytophthora infestans, and its sister species, Phytophthora mirabilis, which is responsible for infection of Mirabilis jalapa, are adapted to protease targets unique to their respective host plants. Amino acid polymorphisms in both the inhibitors and their target proteases underpin this biochemical specialization. Our results link effector specialization to diversification and speciation of this plant pathogen.

  • the Irish Potato Famine pathogen phytophthora infestans translocates the crn8 kinase into host plant cells
    PLOS Pathogens, 2012
    Co-Authors: Tolga O. Bozkurt, Jan Sklenar, Mireille Van Damme, Cahid Cakir, Sebastian Schornack, Alexandra M E Jones, Sophien Kamoun
    Abstract:

    Phytopathogenic oomycetes, such as Phytophthora infestans, secrete an arsenal of effector proteins that modulate plant innate immunity to enable infection. We describe CRN8, a host-translocated effector of P. infestans that has kinase activity in planta. CRN8 is a modular protein of the CRN effector family. The C-terminus of CRN8 localizes to the host nucleus and triggers cell death when the protein is expressed in planta. Cell death induction by CRN8 is dependent on its localization to the plant nucleus, which requires a functional nuclear localization signal (NLS). The C-terminal sequence of CRN8 has similarity to a serine/threonine RD kinase domain. We demonstrated that CRN8 is a functional RD kinase and that its auto-phosphorylation is dependent on an intact catalytic site. Co-immunoprecipitation experiments revealed that CRN8 forms a dimer or multimer. Heterologous expression of CRN8 in planta resulted in enhanced virulence by P. infestans. In contrast, in planta expression of the dominant-negative CRN8R469A;D470A resulted in reduced P. infestans infection, further implicating CRN8 in virulence. Overall, our results indicate that similar to animal parasites, plant pathogens also translocate biochemically active kinase effectors inside host cells.

Jean B. Ristaino - One of the best experts on this subject based on the ideXlab platform.

  • Genomic Characterization of a South American Phytophthora Hybrid Mandates Reassessment of the Geographic Origins of Phytophthora infestans
    Molecular biology and evolution, 2015
    Co-Authors: Michael D. Martin, Filipe G. Vieira, Nathan Wales, Mikkel Schubert, Andaine Seguin-orlando, Jean B. Ristaino, M. Thomas P. Gilbert
    Abstract:

    As the oomycete pathogen causing Potato late blight disease, Phytophthora infestans triggered the famous 19th-century Irish Potato Famine and remains the leading cause of global commercial Potato crop destruction. But the geographic origin of the genotype that caused this devastating initial outbreak remains disputed, as does the New World center of origin of the species itself. Both Mexico and South America have been proposed, generating considerable controversy. Here, we readdress the pathogen’s origins using a genomic data set encompassing 71 globally sourced modern and historical samples of P. infestans and the hybrid species P. andina, a close relative known only from the Andean highlands. Previous studies have suggested that the nuclear DNA lineage behind the initial outbreaks in Europe in 1845 is now extinct. Analysis of P. andina’s phased haplotypes recovered eight haploid genome sequences, four of which represent a previously unknown basal lineage of P. infestans closely related to the Famine-era lineage. Our analyses further reveal that clonal lineages of both P. andina and historical P. infestans diverged earlier than modern Mexican lineages, casting doubt on recent claims of a Mexican center of origin. Finally, we use haplotype phasing to demonstrate that basal branches of the clade comprising Mexican samples are occupied by clonal isolates collected from wild Solanum hosts, suggesting that modern Mexican P. infestans diversified on Solanum tuberosum after a host jump from a wild species and that the origins of P. infestans are more complex than was previously thought.

  • persistence of the mitochondrial lineage responsible for the Irish Potato Famine in extant new world phytophthora infestans
    Molecular Biology and Evolution, 2014
    Co-Authors: Michael D. Martin, Nathan Wales, Jean B. Ristaino, Thomas M P Gilbert
    Abstract:

    The plant pathogen Phytophthora infestans emerged in Europe in 1845, triggering the Irish Potato Famine and massive European Potato crop losses that continued until effective fungicides were widely employed in the 20th century. Today the pathogen is ubiquitous, with more aggressive and virulent strains surfacing in recent decades. Recently, complete P. infestans mitogenome sequences from 19th-century herbarium specimens were shown to belong to a unique lineage (HERB-1) predicted to be rare or extinct in modern times. We report 44 additional P. infestans mitogenomes: four from 19th-century Europe, three from 1950s UK, and 37 from modern populations across the New World. We use phylogenetic analyses to identify the HERB-1 lineage in modern populations from both Mexico and South America, and to demonstrate distinct mitochondrial haplotypes were present in 19th-century Europe, with this lineage initially diversifying 75 years before the first reports of Potato late blight.

  • phylogenetic relationships of phytophthora andina a new species from the highlands of ecuador that is closely related to the Irish Potato Famine pathogen phytophthora infestans
    Mycologia, 2008
    Co-Authors: Luis Gomezalpizar, Ricardo Oliva, Gregory A Forbes, Jean B. Ristaino
    Abstract:

    Phylogenetic relationships of Phytophthora infestans sensu lato in the Andean highlands of South America were examined. Three clonal lineages (US-1, EC-1, EC-3) and one heterogeneous lineage (EC-2) were found in association with different host species in genus Solanum. The EC-2 lineage includes two mitochondrial (mtDNA) haplotypes, Ia and Ic. Isolates of P. infestans sensu lato EC-2 fit the morphological description of P. infestans but are different from any genotypes of P. infestans described to date. All isolates of P. infestans sensu lato from Ecuador were amplified by a P. infestans specific primer (PINF), and restriction fragment length patterns were identical in isolates amplified with ITS primers 4 and 5. The EC-1 clonal lineage of P. infestans sensu lato from S. andreanum, S. columbianum, S. paucijugum, S. phureja, S. regularifolium, S. tuberosum and S. tuquerense was confirmed to be P. infestans based on sequences of the cytochrome oxidase I (cox I) gene and intron 1 of ras gene. The EC-2 isolates with the Ic haplotype formed a distinct branch in the same clade with P. infestans and P. mirabilis, P. phaseoli and P. ipomoeae for both cox I and ras intron 1 phylogenies and were identified as the newly described species P. andina. Ras intron 1 sequence data suggests that P. andina might have arisen via hybridization between P. infestans and P. mirabilis.

  • identity of the mtdna haplotype s of phytophthora infestans in historical specimens from the Irish Potato Famine
    Fungal Biology, 2004
    Co-Authors: Kimberley Jane May, Jean B. Ristaino
    Abstract:

    The mtDNA haplotypes of the plant pathogen Phytophthora infestans present in dried Potato and tomato leaves from herbarium specimens collected during the Irish Potato Famine and later in the 19th and early 20th century were identified. A 100 bp fragment of ribosomal DNA (rDNA) specific for P. infestans was amplified from 90% of the specimens (n = 186), confirming infection by P. infestans. Primers were designed that distinguish the extant mtDNA haplotypes. 86% percent of the herbarium specimens from historic epidemics were infected with the Ia mtDNA haplotype. Two mid-20th century Potato leaves from Ecuador (1967) and Bolivia (1944) were infected with the Ib mtDNA haplotype of the pathogen. Both the Ia and IIb haplotypes were found in specimens collected in Nicaragua in the 1950s. The data suggest that the Ia haplotype of P. infestans was responsible for the historic epidemics during the 19th century in the UK, Europe, and the USA. The Ib mtDNA haplotype of the pathogen was dispersed later in the early 20th century from Bolivia and Ecuador. Multiple haplotypes were present outside Mexico in the 1940s-60s, indicating that pathogen diversity was greater than previously believed.

  • tracking historic migrations of the Irish Potato Famine pathogen phytophthora infestans
    Microbes and Infection, 2002
    Co-Authors: Jean B. Ristaino
    Abstract:

    The plant pathogen Phytophthora infestans causes late blight, a devastating disease on Potato that led to the Irish Potato Famine during 1845-1847. The disease is considered a reemerging problem and still causes major epidemics on both Potato and tomato crops worldwide. Theories on the origin of the disease based on an examination of the genetic diversity and structure of P. infestans populations and use of historic specimens to understand modern day epidemics are discussed.