Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

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    Functional Divergence of Two Secreted Immune Proteases of Tomato
    Ilyas, M. ; Hörger, A.C. ; Bozkurt, T.O. ; Burg, H.A. van den; Kaschani, F. ; Kaiser, M. ; Belhaj, K. ; Smoker, M. ; Joosten, M. ; Kamoun, S. ; Hoorn, R.A.L. van der - \ 2015
    Current Biology 25 (2015)17. - ISSN 0960-9822 - p. 2300 - 2306.
    cf-2-dependent disease resistance - pathogen effectors - transcription factors - provides insights - genome sequence - plant-pathogens - gene - defense - target - specialization
    Rcr3 and Pip1 are paralogous secreted papain-like proteases of tomato. Both proteases are inhibited by Avr2 from the fungal pathogen Cladosporium fulvum, but only Rcr3 acts as a co-receptor for Avr2 recognition by the tomato Cf-2 immune receptor [ 1, 2, 3 and 4]. Here, we show that Pip1-depleted tomato plants are hyper-susceptible to fungal, bacterial, and oomycete plant pathogens, demonstrating that Pip1 is an important broad-range immune protease. By contrast, in the absence of Cf-2, Rcr3 depletion does not affect fungal and bacterial infection levels but causes increased susceptibility only to the oomycete pathogen Phytophthora infestans. Rcr3 and Pip1 reside on a genetic locus that evolved over 36 million years ago. These proteins differ in surface-exposed residues outside the substrate-binding groove, and Pip1 is 5- to 10-fold more abundant than Rcr3. We propose a model in which Rcr3 and Pip1 diverged functionally upon gene duplication, possibly driven by an arms race with pathogen-derived inhibitors or by coevolution with the Cf-2 immune receptor detecting inhibitors of Rcr3, but not of Pip1.
    The battle in the apoplast: further insights into the roles of proteases and their inhibitors in plant-pathogen interactions
    Karimi Jashni, M. ; Mehrabi, R. ; Collemare, J. ; Mesarich, C.H. ; Wit, P.J.G.M. de - \ 2015
    Frontiers in Plant Science 6 (2015). - ISSN 1664-462X - 7 p.
    cf-2-dependent disease resistance - extracellular serine-protease - l. enhances resistance - class iv chitinases - phytophthora-infestans - cladosporium-fulvum - proteolytic-enzymes - antifungal activity - gene-expression - tomato
    Upon host penetration, fungal pathogens secrete a plethora of effectors to promote disease, including proteases that degrade plant antimicrobial proteins, and protease inhibitors (PIs) that inhibit plant proteases with antimicrobial activity. Conversely, plants secrete proteases and PIs to protect themselves against pathogens or to mediate recognition of pathogen proteases and PIs, which leads to induction of defense responses. Many examples of proteases and PIs mediating effector-triggered immunity in host plants have been reported in the literature, but little is known about their role in compromising basal defense responses induced by microbe-associated molecular patterns. Recently, several reports appeared in literature on secreted fungal proteases that modify or degrade pathogenesis-related proteins, including plant chitinases or PIs that compromise their activities. This prompted us to review the recent advances on proteases and PIs involved in fungal virulence and plant defense. Proteases and PIs from plants and their fungal pathogens play an important role in the arms race between plants and pathogens, which has resulted in co-evolutionary diversification and adaptation shaping pathogen lifestyles.
    Apoplastic Venom Allergen-like Proteins of Cyst Nematodes Modulate the Activation of Basal Plant Innate Immunity by Cell Surface Receptors
    Lozano Torres, J.L. ; Wilbers, R.H.P. ; Warmerdam, S. ; Finkers-Tomczak, A.M. ; Diaz Granados Muñoz, A. ; Schaik, C.C. van; Helder, J. ; Bakker, J. ; Goverse, A. ; Schots, A. ; Smant, G. - \ 2014
    PLoS Pathogens 10 (2014)12. - ISSN 1553-7366 - 18 p.
    root-knot nematode - cf-2-dependent disease resistance - pamp-triggered immunity - arabidopsis-thaliana - globodera-rostochiensis - heterodera-schachtii - ancylostoma-caninum - parasitic nematodes - extracellular-matrix - functional-analysis
    Despite causing considerable damage to host tissue during the onset of parasitism, nematodes establish remarkably persistent infections in both animals and plants. It is thought that an elaborate repertoire of effector proteins in nematode secretions suppresses damage-triggered immune responses of the host. However, the nature and mode of action of most immunomodulatory compounds in nematode secretions are not well understood. Here, we show that venom allergen-like proteins of plant-parasitic nematodes selectively suppress host immunity mediated by surface-localized immune receptors. Venom allergen-like proteins are uniquely conserved in secretions of all animal- and plant-parasitic nematodes studied to date, but their role during the onset of parasitism has thus far remained elusive. Knocking-down the expression of the venom allergen-like protein Gr-VAP1 severely hampered the infectivity of the potato cyst nematode Globodera rostochiensis. By contrast, heterologous expression of Gr-VAP1 and two other venom allergen-like proteins from the beet cyst nematode Heterodera schachtii in plants resulted in the loss of basal immunity to multiple unrelated pathogens. The modulation of basal immunity by ectopic venom allergen-like proteins in Arabidopsis thaliana involved extracellular protease-based host defenses and non-photochemical quenching in chloroplasts. Non-photochemical quenching regulates the initiation of the defense-related programmed cell death, the onset of which was commonly suppressed by venom allergen-like proteins from G. rostochiensis, H. schachtii, and the root-knot nematode Meloidogyne incognita. Surprisingly, these venom allergen-like proteins only affected the programmed cell death mediated by surface-localized immune receptors. Furthermore, the delivery of venom allergen-like proteins into host tissue coincides with the enzymatic breakdown of plant cell walls by migratory nematodes. We, therefore, conclude that parasitic nematodes most likely utilize venom allergen-like proteins to suppress the activation of defenses by immunogenic breakdown products in damaged host tissue.
    Transcriptome sequencing uncovers the Avr5 avirulence gene of the tomato leaf mould pathogen Cladosporium fulvum
    Mesarich, C.H. ; Griffiths, S.A. ; Burgt, A. van der; Okmen, B. ; Beenen, H. ; Etalo, D.W. ; Joosten, M.H.A.J. ; Wit, P.J.G.M. de - \ 2014
    Molecular Plant-Microbe Interactions 27 (2014)8. - ISSN 0894-0282 - p. 846 - 857.
    fungal effector proteins - cf-2-dependent disease resistance - aspergillus-nidulans - secreted proteins - candidate effectors - neurospora-crassa - allelic variation - virulence factor - signal peptides - plant-pathogens
    The Cf-5 gene of tomato confers resistance to strains of the fungal pathogen Cladosporium fulvum carrying the avirulence gene Avr5. Although Cf-5 has been cloned, Avr5 has remained elusive. We report the cloning of Avr5 using a combined bioinformatic and transcriptome sequencing approach. RNA-Seq was performed on the sequenced race 0 strain (0WU; carrying Avr5), as well as a race 5 strain (IPO 1979; lacking a functional Avr5 gene) during infection of susceptible tomato. Forty-four in planta–induced C. fulvum candidate effector (CfCE) genes of 0WU were identified that putatively encode a secreted, small cysteine-rich protein. An expressed transcript sequence comparison between strains revealed two polymorphic CfCE genes in IPO 1979. One of these conferred avirulence to IPO 1979 on Cf-5 tomato following complementation with the corresponding 0WU allele, confirming identification of Avr5. Complementation also led to increased fungal biomass during infection of susceptible tomato, signifying a role for Avr5 in virulence. Seven of eight race 5 strains investigated escape Cf-5-mediated resistance through deletion of the Avr5 gene. Avr5 is heavily flanked by repetitive elements, suggesting that repeat instability, in combination with Cf-5-mediated selection pressure, has led to the emergence of race 5 strains deleted for the Avr5 gene.
    Effector-triggered defence against apoplastic fungal pathogens
    Stotz, H.U. ; Mitrousia, G.K. ; Wit, P.J.G.M. de; Fitt, B.D.L. - \ 2014
    Trends in Plant Science 19 (2014)8. - ISSN 1360-1385 - p. 491 - 500.
    programmed cell-death - plant immune-system - cf-2-dependent disease resistance - leptosphaeria-maculans - cladosporium-fulvum - brassica-napus - mycosphaerella-graminicola - avirulence gene - rhynchosporium-secalis - oilseed rape
    R gene-mediated host resistance against apoplastic fungal pathogens is not adequately explained by the terms pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) or effector-triggered immunity (ETI). Therefore, it is proposed that this type of resistance is termed 'effector-triggered defence' (ETD). Unlike PTI and ETI, ETD is mediated by R genes encoding cell surface-localised receptor-like proteins (RLPs) that engage the receptor-like kinase SOBIR1. In contrast to this extracellular recognition, ETI is initiated by intracellular detection of pathogen effectors. ETI is usually associated with fast, hypersensitive host cell death, whereas ETD often triggers host cell death only after an elapsed period of endophytic pathogen growth. In this opinion, we focus on ETD responses against foliar fungal pathogens of crops.
    The Activation and Suppression of Plant Innate Immunity by Parasitic Nematodes
    Goverse, A. ; Smant, G. - \ 2014
    Annual Review of Phytopathology 52 (2014). - ISSN 0066-4286 - p. 243 - 265.
    root-knot nematode - potato cyst-nematode - cf-2-dependent disease resistance - expressed sequence tags - globodera-rostochiensis - heterodera-glycines - arabidopsis-thaliana - mi-1-mediated resistance - meloidogyne-incognita - signaling pathway
    Plant-parasitic nematodes engage in prolonged and intimate relationships with their host plants, often involving complex alterations in host cell morphology and function. It is puzzling how nematodes can achieve this, seemingly without activating the innate immune system of their hosts. Secretions released by infective juvenile nematodes are thought to be crucial for host invasion, for nematode migration inside plants, and for feeding on host cells. In the past, much of the research focused on the manipulation of developmental pathways in host plants by plant-parasitic nematodes. However, recent findings demonstrate that plant-parasitic nematodes also deliver effectors into the apoplast and cytoplasm of host cells to suppress plant defense responses. In this review, we describe the current insights in the molecular and cellular mechanisms underlying the activation and suppression of host innate immunity by plant-parasitic nematodes along seven critical evolutionary and developmental transitions in plant parasitism.
    Affinity of Avr2 for tomato cysteine protease Rcr3 correlates with the Avr2-triggered Cf-2-mediated hypersensitive response
    Klooster, J.W. van t; Kamp, M.W. van der; Vervoort, J.J.M. ; Beekwilder, J. ; Boeren, S. ; Joosten, M.H.A.J. ; Thomma, B.P.H.J. ; Wit, P.J.G.M. de - \ 2011
    Molecular Plant Pathology 12 (2011)1. - ISSN 1464-6722 - p. 21 - 30.
    pathogen cladosporium-fulvum - cf-2-dependent disease resistance - fungal effector proteins - race-specific elicitor - avirulence gene avr9 - virulence factor - plant proteases - pichia-pastoris - binding-site - cystine knot
    The Cladosporium fulvum Avr2 effector is a novel type of cysteine protease inhibitor with eight cysteine residues that are all involved in disulphide bonds. We have produced wild-type Avr2 protein in Pichia pastoris and determined its disulphide bond pattern. By site-directed mutagenesis of all eight cysteine residues, we show that three of the four disulphide bonds are required for Avr2 stability. The six C-terminal amino acid residues of Avr2 contain one disulphide bond that is not embedded in its overall structure. Avr2 is not processed by the tomato cysteine protease Rcr3 and is an uncompetitive inhibitor of Rcr3. We also produced mutant Avr2 proteins in which selected amino acid residues were individually replaced by alanine, and, in one mutant, all six C-terminal amino acid residues were deleted. We determined the inhibitory constant (Ki) of these mutants for Rcr3 and their ability to trigger a Cf-2-mediated hypersensitive response (HR) in tomato. We found that the two C-terminal cysteine residues and the six amino acid C-terminal tail of Avr2 are required for both Rcr3 inhibitory activity and the ability to trigger a Cf-2-mediated HR. Individual replacement of the lysine-17, lysine-20 or tyrosine-21 residue by alanine did not affect significantly the biological activity of Avr2. Overall, our data suggest that the affinity of the Avr2 mutants for Rcr3 correlates with their ability to trigger a Cf-2-mediated HR
    The Diverse Roles of Extracellular Leucine-rich Repeat-containing Receptor-like Proteins in Plants
    Wang, G. ; Fiers, M.A. ; Ellendorff, U. ; Wang, Z. ; Wit, P.J.G.M. de; Angenent, G.C. ; Thomma, B.P.H.J. - \ 2010
    Critical Reviews in Plant Sciences 29 (2010). - ISSN 0735-2689 - p. 285 - 299.
    stem-cell fate - cf-2-dependent disease resistance - arabidopsis shoot meristems - ligand-induced endocytosis - of-function phenotypes - apple scab disease - cladosporium-fulvum - organ development - hypersensitive response - root-meristem
    Plant cells use various types of cell surface receptor molecules to sense extracellular signals and modulate cell-to-cell communication in many biological processes. Extracellular leucine-rich repeat (eLRR) receptor-like proteins (RLPs) represent an important class of such cell surface receptors. RLPs differ from receptor-like kinases (RLKs), which compose the largest class of cell surface receptors in many plant species, because they lack a cytoplasmic kinase domain. RLPs play roles in both developmental processes and disease resistance. A total of 57 RLP encoding genes has been identified in Arabidopsis. Two of them, CLAVATA2 (CLV2) and Too Many Mouths (TMM) have a function in meristem maintenance and stomatal distribution, respectively, whereas few others act in basal defense against pathogens. Although the function of most RLPs in Arabidopsis remains unclear, considerable progress has been made in understanding RLP functioning and signaling over the years. This review focuses on the function of RLPs in plants. Furthermore, the function of distinct RLP domains and the role of conserved residues important for perception and ligand specificity are discussed. The role of RLP proteins in multimeric complexes to sense biotic and abiotic extracellular signals is also addressed.
    Rin4 Causes Hybrid Necrosis and Race-Specific Resistance in an Interspecific Lettuce Hybrid
    Jeuken, M.J.W. ; Zhang, N. ; McHale, L.K. ; Pelgrom, K.T.B. ; Boer, E. den; Lindhout, P. ; Michelmore, R. ; Visser, R.G.F. ; Niks, R.E. - \ 2009
    The Plant Cell 21 (2009)10. - ISSN 1040-4651 - p. 3368 - 3378.
    cf-2-dependent disease resistance - backcross inbred lines - lactuca-saligna - bremia-lactucae - nonhost resistance - effector avrrpt2 - gene-expression - downy mildew - wild lettuce - arabidopsis
    Some inter- and intraspecific crosses may result in reduced viability or sterility in the offspring, often due to genetic incompatibilities resulting from interactions between two or more loci. Hybrid necrosis is a postzygotic genetic incompatibility that is phenotypically manifested as necrotic lesions on the plant. We observed hybrid necrosis in interspecific lettuce (Lactuca sativa and Lactuca saligna) hybrids that correlated with resistance to downy mildew. Segregation analysis revealed a specific allelic combination at two interacting loci to be responsible. The allelic interaction had two consequences: (1) a quantitative temperature-dependent autoimmunity reaction leading to necrotic lesions, lethality, and quantitative resistance to an otherwise virulent race of Bremia lactucae; and (2) a qualitative temperature-independent race-specific resistance to an avirulent race of B. lactucae. We demonstrated by transient expression and silencing experiments that one of the two interacting genes was Rin4. In Arabidopsis thaliana, RIN4 is known to interact with multiple R gene products, and their interactions result in hypersensitive resistance to Pseudomonas syringae. Site-directed mutation studies on the necrosis-eliciting allele of Rin4 in lettuce showed that three residues were critical for hybrid necrosis
    Fungal effector proteins: past, present and future
    Wit, P.J.G.M. de; Mehrabi, R. ; Burg, H.A. van den; Stergiopoulos, I. - \ 2009
    Molecular Plant Pathology 10 (2009)6. - ISSN 1464-6722 - p. 735 - 747.
    pathogen cladosporium-fulvum - rice blast resistance - avirulence gene avr9 - cf-2-dependent disease resistance - powdery mildew resistance - race-specific elicitor - magnaporthe-grisea - leptosphaeria-maculans - fusarium-oxysporum - flax rust
    The pioneering research of Harold Flor on flax and the flax rust fungus culminated in his gene-for-gene hypothesis. It took nearly 50 years before the first fungal avirulence (Avr) gene in support of his hypothesis was cloned. Initially, fungal Avr genes were identified by reverse genetics and map-based cloning from model organisms, but, currently, the availability of many sequenced fungal genomes allows their cloning from additional fungi by a combination of comparative and functional genomics. It is believed that most Avr genes encode effectors that facilitate virulence by suppressing pathogen-associated molecular pattern-triggered immunity and induce effector-triggered immunity in plants containing cognate resistance proteins. In resistant plants, effectors are directly or indirectly recognized by cognate resistance proteins that reside either on the plasma membrane or inside the plant cell. Indirect recognition of an effector (also known as the guard model) implies that the virulence target of an effector in the host (the guardee) is guarded by the resistance protein (the guard) that senses manipulation of the guardee, leading to activation of effector-triggered immunity. In this article, we review the literature on fungal effectors and some pathogen-associated molecular patterns, including those of some fungi for which no gene-for-gene relationship has been established.
    Fungal effector proteins
    Stergiopoulos, I. ; Wit, P.J.G.M. de - \ 2009
    Annual Review of Phytopathology 47 (2009). - ISSN 0066-4286 - p. 233 - 263.
    pathogen cladosporium-fulvum - rice blast resistance - avirulence gene avr9 - flax rust resistance - cf-2-dependent disease resistance - powdery mildew resistance - race-specific elicitor - f-sp hordei - magnaporthe-grisea - rhynchosporium-secalis
    It is accepted that most fungal avirulence genes encode virulence factors that are called effectors. Most fungal effectors are secreted, cysteine-rich proteins, and a role in virulence has been shown for a few of them, including Avr2 and Avr4 of Cladosporium fulvum, which inhibit plant cysteine proteases and protect chitin in fungal cell walls against plant chitinases, respectively. In resistant plants, effectors are directly or indirectly recognized by cognate resistance proteins that reside either inside the plant cell or on plasma membranes. Several secreted effectors function inside the host cell, but the uptake mechanism is not yet known. Variation observed among fungal effectors shows two types of selection that appear to relate to whether they interact directly or indirectly with their cognate resistance proteins. Direct interactions seem to favor point mutations in effector genes, leading to amino acid substitutions, whereas indirect interactions seem to favor jettison of effector genes.
    RD19, an Arabidopsis cysteine protease required for RRS1-R-mediated resistance, is relocalized to the nucleus by the Ralstonia solanacearum PopP2 effector
    Bernoux, M. ; Timmers, T. ; Jauneau, A. ; Brière, C. ; Wit, P.J.G.M. de; Marco, Y. ; Deslandes, L. - \ 2008
    The Plant Cell 20 (2008)8. - ISSN 1040-4651 - p. 2252 - 2264.
    agrobacterium-mediated transformation - cf-2-dependent disease resistance - tomato lycopersicon-esculentum - lifetime imaging microscopy - programmed cell-death - plant innate immunity - for-gene concept - iii effector - cladosporium-fulvum - hypersensitive respon
    Bacterial wilt, a disease impacting cultivated crops worldwide, is caused by the pathogenic bacterium Ralstonia solanacearum. PopP2 (for Pseudomonas outer protein P2) is an R. solanacearum type III effector that belongs to the YopJ/AvrRxv protein family and interacts with the Arabidopsis thaliana RESISTANT TO RALSTONIA SOLANACEARUM 1-R (RRS1-R) resistance protein. RRS1-R contains the Toll/Interleukin1 receptor¿nucleotide binding site¿Leu-rich repeat domains found in several cytoplasmic R proteins and a C-terminal WRKY DNA binding domain. In this study, we identified the Arabidopsis Cys protease RESPONSIVE TO DEHYDRATION19 (RD19) as being a PopP2-interacting protein whose expression is induced during infection by R. solanacearum. An Arabidopsis rd19 mutant in an RRS1-R genetic background is compromised in resistance to the bacterium, indicating that RD19 is required for RRS1-R¿mediated resistance. RD19 normally localizes in mobile vacuole-associated compartments and, upon coexpression with PopP2, is specifically relocalized to the plant nucleus, where the two proteins physically interact. No direct physical interaction between RRS1-R and RD19 in the presence of PopP2 was detected in the nucleus as determined by Förster resonance energy transfer. We propose that RD19 associates with PopP2 to form a nuclear complex that is required for activation of the RRS1-R¿mediated resistance response.
    The Cladosporium fulvum virulence protein Avr2 inhibits host proteases required for basal defense
    Esse, H.P. van; Klooster, J.W. van t; Bolton, M.D. ; Yadeta, K.A. ; Baarlen, P. van; Boeren, S. ; Vervoort, J.J.M. ; Wit, P.J.G.M. de; Thomma, B.P.H.J. - \ 2008
    The Plant Cell 20 (2008)7. - ISSN 1040-4651 - p. 1948 - 1963.
    programmed cell-death - cf-2-dependent disease resistance - syringae effector avrrpt2 - caspase-like activity - avirulence gene avr9 - arabidopsis-thaliana - hypersensitive response - cysteine proteases - plant-pathogen - molecular-mechanisms
    Cladosporium fulvum (syn. Passalora fulva) is a biotrophic fungal pathogen that causes leaf mold of tomato (Solanum lycopersicum). During growth in the apoplast, the fungus establishes disease by secreting effector proteins, 10 of which have been characterized. We have previously shown that the Avr2 effector interacts with the apoplastic tomato Cys protease Rcr3, which is required for Cf-2¿mediated immunity. We now show that Avr2 is a genuine virulence factor of C. fulvum. Heterologous expression of Avr2 in Arabidopsis thaliana causes enhanced susceptibility toward extracellular fungal pathogens, including Botrytis cinerea and Verticillium dahliae, and microarray analysis showed that Avr2 expression triggers a global transcriptome reflecting pathogen challenge. Cys protease activity profiling showed that Avr2 inhibits multiple extracellular Arabidopsis Cys proteases. In tomato, Avr2 expression caused enhanced susceptibility toward Avr2-defective C. fulvum strains and also toward B. cinerea and V. dahliae. Cys protease activity profiling in tomato revealed that, in this plant also, Avr2 inhibits multiple extracellular Cys proteases, including Rcr3 and its close relative Pip1. Finally, silencing of Avr2 significantly compromised C. fulvum virulence on tomato. We conclude that Avr2 is a genuine virulence factor of C. fulvum that inhibits several Cys proteases required for plant basal defense.
    The novel Cladosporium fulvum lysin motif effector Ecp6 is a virulence factor with orthologues in other fungal species
    Bolton, M.D. ; Esse, H.P. van; Vossen, J.H. ; Jonge, R. de; Stergiopoulos, I. ; Stulemeijer, I.J.E. ; Berg, G.C.M. van den; Borrás-Hidalgo, O. ; Dekker, H.L. ; Koster, C.G. de; Wit, P.J.G.M. de; Joosten, M.H.A.J. ; Thomma, B.P.H.J. - \ 2008
    Molecular Microbiology 69 (2008)1. - ISSN 0950-382X - p. 119 - 136.
    cf-2-dependent disease resistance - receptor-like kinases - avirulence gene avr9 - plant-pathogen - agrobacterium-tumefaciens - cf-4-mediated resistance - phytopathogenic bacteria - extracellular proteins - pseudomonas-syringae - bacillus-subtilis
    During tomato leaf colonization, the biotrophic fungus Cladosporium fulvum secretes several effector proteins into the apoplast. Eight effectors have previously been characterized and show no significant homology to each other or to other fungal genes. To discover novel C. fulvum effectors that might play a role in virulence, we utilized two-dimensional polyacrylamide gel electrophoresis (2D-PAGE) to visualize proteins secreted during C. fulvum-tomato interactions. Three novel C. fulvum proteins were identified: CfPhiA, Ecp6 and Ecp7. CfPhiA shows homology to proteins found on fungal sporogenous cells called phialides. Ecp6 contains lysin motifs (LysM domains) that are recognized as carbohydrate-binding modules. Ecp7 encodes a small, cysteine-rich protein with no homology to known proteins. Heterologous expression of Ecp6 significantly increased the virulence of the vascular pathogen Fusarium oxysporum on tomato. Furthermore, by RNA interference (RNAi)-mediated gene silencing we demonstrate that Ecp6 is instrumental for C. fulvum virulence on tomato. Hardly any allelic variation was observed in the Ecp6 coding region of a worldwide collection of C. fulvum strains. Although none of the C. fulvum effectors identified so far have obvious orthologues in other organisms, conserved Ecp6 orthologues were identified in various fungal species. Homology-based modelling suggests that the LysM domains of C. fulvum Ecp6 may be involved in chitin binding.
    Allelic variation in the effector genes of the tomato pathogen Cladosporium fulvum reveals different modes of adaptive evolution
    Stergiopoulos, I. ; Kock, M.J.D. de; Lindhout, P. ; Wit, P.J.G.M. de - \ 2007
    Molecular Plant-Microbe Interactions 20 (2007)10. - ISSN 0894-0282 - p. 1271 - 1283.
    amino-acid sites - cf-2-dependent disease resistance - avirulence gene - plant-pathogen - cf-4-mediated resistance - extracellular proteins - positive selection - virulence factor - fungal pathogen - downy mildew
    The allelic variation in four avirulence (Avr) and four extracellular protein (Ecp)¿encoding genes of the tomato pathogen Cladosporium fulvum was analyzed for a worldwide collection of strains. The majority of polymorphisms observed in the Avr genes are deletions, point mutations, or insertions of transposon-like elements that are associated with transitions from avirulence to virulence, indicating adaptive evolution of the Avr genes to the cognate C. fulvum resistance genes that are deployed in commercial tomato lines. Large differences in types of polymorphisms between the Avr genes were observed, especially between Avr2 (indels) and Avr4 (amino-acid substitutions), indicating that selection pressure favors different types of adaptation. In contrast, only a limited number of polymorphisms were observed in the Ecp genes, which mostly involved synonymous modifications. A haplotype network based on the polymorphisms observed in the effector genes revealed a complex pattern of evolution marked by reticulations that suggests the occurrence of genetic recombination in this presumed asexual fungus. This, as well as the identification of strains with identical polymorphisms in Avr and Ecp genes but with opposite mating-type genes, suggests that development of complex races can be the combined result of positive selection and genetic recombination.
    Cladosporium fulvum Avr4 protects fungal cell walls against hydrolysis by plant chitinases accumulating during infection
    Burg, H.A. van den; Harrison, S.J. ; Joosten, M.H.A.J. ; Vervoort, J.J.M. ; Wit, P.J.G.M. de - \ 2006
    Molecular Plant-Microbe Interactions 19 (2006)12. - ISSN 0894-0282 - p. 1420 - 1430.
    pathogenesis-related proteins - cf-2-dependent disease resistance - carbohydrate-binding modules - race-specific elicitor - subcellular-localization - tomato leaves - cf-4-mediated resistance - magnaporthe-grisea - protease inhibitor - avirulence gene
    Resistance against the leaf mold fungus Cladosporium fulvum is mediated by the tomato Cf proteins which belong to the class of receptor-like proteins and indirectly recognize extracellular avirulence proteins (Avrs) of the fungus. Apart from triggering disease resistance, Avrs are believed to play a role in pathogenicity or virulence of C. fulvum. Here, we report on the avirulence protein Avr4, which is a chitin-binding lectin containing an invertebrate chitin-binding domain (CBM14). This domain is found in many eukaryotes, but has not yet been described in fungal or plant genomes. We found that interaction of Avr4 with chitin is specific, because it does not interact with other cell wall polysaccharides. Avr4 binds to chitin oligomers with a minimal length of three N-acetyl glucosamine residues. In vitro, Avr4 protects chitin against hydrolysis by plant chitinases. Avr4 also binds to chitin in cell walls of the fungi Trichoderma viride and Fusarium solani f. sp. phaseoli and protects these fungi against normally deleterious concentrations of plant chitinases. In situ fluorescence studies showed that Avr4 also binds to cell walls of C. fulvum during infection of tomato, where it most likely protects the fungus against tomato chitinases, suggesting that Avr4 is a counter-defensive virulence factor.
    Affinity-tags are removed from Cladosporium fulvum effector proteins expressed in the tomato leaf apoplast
    Esse, H.P. van; Thomma, B.P.H.J. ; Klooster, J.W. van t; Wit, P.J.G.M. de - \ 2006
    Journal of Experimental Botany 57 (2006)3. - ISSN 0022-0957 - p. 599 - 608.
    cf-2-dependent disease resistance - cf-4-mediated resistance - locus comprises - cf-4 locus - pathogen - gene - avr9 - purification - elicitor - identification
    Cladosporium fulvum (syn. Passalora fulva) is a biotrophic fungal pathogen that causes leaf mould on tomato (Solanum esculentum). The fungus grows exclusively in the tomato leaf apoplast where it secretes several small (
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