Studies on infection mechanisms of oomycete plant pathogens
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Studies on infection mechanisms of oomycete plant pathogens Shuta Asai1 Received: 4 August 2020 / Accepted: 16 August 2020 © The Phytopathological Society of Japan and Springer Japan KK, part of Springer Nature 2020
Introduction Plants and pathogens have co-evolved in a defensive–offensive battle for survival. Plants induce basal resistance by sensing broadly conserved pathogen molecules. On the other hand, pathogens have produced effectors that act as a virulence factor and have acquired the ability to infect plants by suppressing their basal resistance (Asai and Shirasu 2015). In turn, plants have evolved intracellular receptors called resistance (R) genes, which recognize the presence of pathogen effectors directly or indirectly to launch a strong counterattack (Jones and Dangl 2006). By clarifying the functions and host targets of effectors, therefore, we have expected to identify important factors involved in plant immunity. Pathogen effectors have evolved to evade recognition by R genes. Therefore, if the recognition avoidance mechanism can be elucidated, the determinant mechanism of infection will become clear, which will be the basis for developing disease-control methods in the future. Hyaloperonospora arabidopsidis (Hpa) is an obligate biotrophic oomycete that causes downy mildew in Arabidopsis thaliana (hereafter, Arabidopsis). A number of putative Hpa effectors capable of suppressing plant immune responses have been identified (Fabro et al. 2011), but their host targets and the mechanisms of plant immune suppression have been unknown.
This article is an abstract of the paper which was going to be presented by a winner of the Young Scientist Award at the 2020 Annual Meeting of the Phytopathological Society of Japan in Kagoshima. * Shuta Asai [email protected] 1
Center for Sustainable Resource Science, RIKEN, 1‑7‑22, Suehiro‑cho, Tsurumi‑ku, Yokohama, Kanagawa 230‑0045, Japan
Recognition avoidance mechanisms in downy mildew Focusing on the Arabidopsis–Hpa interaction, we established a system to quantify changes in gene expression in both Arabidopsis and Hpa simultaneously during infection (Asai et al. 2014). On the basis of transcriptome data in Arabidopsis Col-0 inoculated with the avirulent Hpa isolate Emoy2 (recognized by RPP4; van der Biezen et al. 2002) or the virulent isolate Waco9, we found that ATR1 (recognized by RPP1; Rehmany et al. 2005) is not expressed in Hpa Waco9. After resequencing the Waco9 genome, we found that the ATR1 region is deleted, leading to evasion of recognition by its cognate R gene, RPP1 (Asai et al. 2014). Comparative genomics and transcriptomics of different isolates of Hpa uncovered the Hpa effector AvrRPP4 recognized by the R gene RPP4 of Arabidopsis (Asai et al. 2018). By investigating Hpa isolates that evade recognition, we also revealed two mechanisms for evading recognition: suppressing effector gene expression or altering its localization in host cells.
Mechanisms of plant immune suppression by downy mildew effectors By histochemical analysis, we fo
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