ORCID Profile
0000-0002-8160-4556
Current Organisations
Wageningen University & Research
,
Wageningen University
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Publisher: Wiley
Date: 03-05-2000
DOI: 10.1111/J.1469-8137.2011.03736.X
Abstract: • A detailed molecular understanding of how oomycete plant pathogens evade disease resistance is essential to inform the deployment of durable resistance (R) genes. • Map-based cloning, transient expression in planta, pathogen transformation and DNA sequence variation across erse isolates were used to identify and characterize PiAVR2 from potato late blight pathogen Phytophthora infestans. • PiAVR2 is an RXLR-EER effector that is up-regulated during infection, accumulates at the site of haustoria formation, and is recognized inside host cells by potato protein R2. Expression of PiAVR2 in a virulent P. infestans isolate conveys a gain-of-avirulence phenotype, indicating that this is a dominant gene triggering R2-dependent disease resistance. PiAVR2 presence/absence polymorphisms and differential transcription explain virulence on R2 plants. Isolates infecting R2 plants express PiAVR2-like, which evades recognition by R2. PiAVR2 and PiAVR2-like differ in 13 amino acids, eight of which are in the C-terminal effector domain one or more of these determines recognition by R2. Nevertheless, few polymorphisms were observed within each gene in pathogen isolates, suggesting limited selection pressure for change within PiAVR2 and PiAVR2-like. • Our results direct a search for R genes recognizing PiAVR2-like, which, deployed with R2, may exert strong selection pressure against the P. infestans population.
Publisher: Wiley
Date: 20-09-2006
DOI: 10.1111/J.1364-3703.2006.00355.X
Abstract: SUMMARY We adapted and optimized the use of the Agrobacterium tumefaciens binary PVX expression system (PVX agroinfection) to screen Solanum plants for response to pathogen elicitors and applied the assay to identify a total of 11 clones of Solanum huancabambense and Solanum microdontum, out of 31 species tested, that respond to the elicitins INF1, INF2A and INF2B of Phytophthora infestans. Prior to this study, response to INF elicitins was only known in Nicotiana spp. within the Solanaceae. The identified S. huancabambense and S. microdontum clones also exhibited hypersensitivity-like cell death following infiltration with purified recombinant INF1, INF2A and INF2B, thereby validating the screening protocol. Comparison of INF elicitin activity revealed that Nicotiana plants responded to significantly lower concentrations than Solanum, suggesting variable levels of sensitivity to INF elicitins. We exploited natural variation in response to INF elicitins in the identified Solanum accessions to evaluate the relationship between INF recognition and late blight resistance. Interestingly, several INF-responsive Solanum plants were susceptible to P. infestans. Also, an S. microdontum xSolanum tuberosum (potato) population that segregates for INF response was generated but failed to identify a measurable contribution of INF response to resistance. These results suggest that in Solanum, INF elicitins are recognized as general elicitors and do not have a measurable contribution to disease resistance.
Publisher: Wiley
Date: 19-08-2021
DOI: 10.1111/NPH.17660
Abstract: Knowledge of the evolutionary processes which govern pathogen recognition is critical to understanding durable disease resistance. We determined how Phytophthora infestans effector Pi AVR2 is recognised by evolutionarily distinct resistance proteins R2 and Rpi‐mcq1. We employed yeast two‐hybrid, co‐immunoprecipitation, virus‐induced gene silencing, transient overexpression, and phosphatase activity assays to investigate the contributions of BSL phosphatases to R2‐ and Rpi‐mcq1‐mediated hypersensitive response (R2 HR and Rpi‐mcq1 HR, respectively). Silencing Pi AVR2 target BSL1 compromises R2 HR. Rpi‐mcq1 HR is compromised only when BSL2 and BSL3 are silenced. BSL1 overexpression increases R2 HR and compromises Rpi‐mcq1. However, overexpression of BSL2 or BSL3 enhances Rpi‐mcq1 and compromises R2 HR. Okadaic acid, which inhibits BSL phosphatase activity, suppresses both recognition events. Moreover, expression of a BSL1 phosphatase‐dead (PD) mutant suppresses R2 HR, whereas BSL2‐PD and BSL3‐PD mutants suppress Rpi‐mcq1 HR. R2 interacts with BSL1 in the presence of PiAVR2, but not with BSL2 and BSL3, whereas no interactions were detected between Rpi‐mcq1 and BSLs. Thus, BSL1 activity and association with R2 determine recognition of Pi AVR2 by R2, whereas BSL2 and BSL3 mediate Rpi‐mcq1 perception of Pi AVR2. R2 and Rpi‐mcq1 utilise distinct mechanisms to detect Pi AVR2 based on association with different BSLs, highlighting central roles of these effector targets for both disease and disease resistance.
Publisher: Oxford University Press (OUP)
Date: 08-2012
No related grants have been discovered for Vivianne Vleeshouwers.