Reactive oxygen species (ROS) play a vital role in plant immune response, but the genes involved in the regulation of ROS are scantily reported. Phytophthora pathogens produce a large number of effectors to promote infection, but the modes of action adopted are largely unknown. Here, we report that RxLR207 could activate ROS-mediated cell death in Nicotiana benthamiana and was essential for virulence of P. capsici. We found that this effector targeted BPA1 (binding partner of ACD11) and four members of BPLs (BPA1-Like proteins) in Arabidopsis, and the bpa1 and bpl mutants had enhanced ROS accumulation and cell death under biotic or abiotic stresses. Furthermore, we showed that BPA1 and several BPLs functioned redundantly in plant immunity to P. capsici. We discovered that BPA1 and all six BPLs interacted with ACD11, and stabilization of ACD11 was impaired in the bpa1, bpl2, bpl3, and bpl4 mutants. RxLR207 could promote the degradation of BPA1, BPL1, BPL2, and BPL4 to disrupt ACD11 stabilization in a 26S proteasome-dependent manner. Taken together, these findings indicate the important roles of Arabidopsis BPA1 and its homologs in ROS homeostasis and defense response, highlighting the usefulness of a pathogen effector-directed approach as a promising strategy for the discovery of novel plant immune regulators.
Even if urban catchments are adequately drained by sewer infrastructures, flooding hotspots develop where ongoing development and poor coordination among utilities conspire with land use and land cover, drainage, and rainfall. We combined spatially explicit land use/land cover data from Luohe City (central China) with soil hydrology (as measured, green space hydraulic conductivity), topography, and observed chronic flooding to analyze the relationships between spatial patterns in pervious surface and flooding. When compared to spatial–structural metrics of land use/cover where flooding was commonly observed, we found that some areas expected to remain dry (given soil and elevation characteristics) still experienced localized flooding, indicating hotspots with overwhelmed sewer infrastructure and a lack of pervious surfaces to effectively infiltrate and drain rainfall. Next, we used curve numbers to represent the composite hydrology of different land use/covers within both chronic flooding and dry (non-flooding) circles of 750 m diameter, and local design storms to determine the anticipated average proportion of runoff. We found that dry circles were more permeable (curve number (mean ± std. error) = 74 ± 2, n = 25) than wetter, flooded circles (curve number = 87 ± 1). Given design storm forcing (20, 50, 100 years’ recurrence interval, and maximum anticipated storm depths), dry points would produce runoff of 26 to 35 percent rainfall, and wet points of 52 to 61 percent of applied rainfall. However, we estimate by simulation that runoff reduction benefits would decline once infiltration-excess (Hortonian) runoff mechanisms activate for storms with precipitation rates in excess of an average of 21 mm/h, contingent on antecedent moisture conditions. Our spatial metrics indicate that larger amounts and patches of dispersed green space mitigate flooding risk, while aggregating buildings (roofs) and green space into larger, separate areas exacerbates risk.
EDS1 (Enhanced Disease Susceptibility 1) plays a crucial role in both effector‐triggered immunity activation and plant basal defence. However, whether pathogen effectors can target EDS1 or an EDS1‐related pathway to manipulate immunity is rarely reported. In this study, we identified a Phytophthora capsici Avirulence Homolog (Avh) RxLR (Arg‐any amino acid‐Leu‐Arg) effector PcAvh103 that interacts with EDS1. We demonstrated that PcAvh103 can facilitate P. capsici infection and is required for pathogen virulence. Furthermore, genetic evidence showed that PcAvh103 contributes to virulence through targeting EDS1. Finally, PcAvh103 specifically interacts with the lipase domain of EDS1 and can promote the disassociation of EDS1–PAD4 (Phytoalexin Deficient 4) complex in planta. Together, our results revealed that the P. capsici RxLR effector PcAvh103 targets host EDS1 to suppress plant immunity, probably through disrupting the EDS1–PAD4 immune signalling pathway.
Phytophthora comprises a group of filamentous plant pathogens that cause serious crop diseases worldwide. It is widely known that a complex effector repertoire was secreted by Phytophthora pathogens to manipulate plant immunity and determine resistance and susceptibility. It is also recognized that Phytophthora pathogens may inhabit natural niches within complex environmental microbes, including bacteria. However, how Phytophthora pathogens interact with their cohabited microbes remains poorly understood. Here, we present such an intriguing case by using Phytophthora –bacteria interaction as a working system. We found that under co-culture laboratory conditions, several Phytophthora pathogens appeared to block the contact of an ecologically relevant bacterium, including Pseudomonas fluorescence and a model bacterium, Escherichia coli . We further observed that Phytophthora sojae utilizes a conserved Crinkler (CRN) effector protein, PsCRN63, to impair bacterial growth. Phytophthora capsici deploys another CRN effector, PcCRN173, to interfere with bacterial flagellum- and/or type IV pilus-mediated motility whereas a P. capsici -derived RxLR effector, PcAvh540, inhibits bacterial swimming motility, but not twitching motility and biofilm formation, suggesting functional diversification of effector-mediated Phytophthora –bacteria interactions. Thus, our studies provide a first case showing that the filamentous Phytophthora pathogens could deploy effectors to interfere with bacterial growth and motility, revealing an unprecedented effector-mediated inter-kingdom interaction between Phytophthora pathogens and bacterial species and thereby uncovering ecological significance of effector proteins in filamentous plant pathogens besides their canonical roles involving pathogen–plant interaction.
Due to their sessile nature, plant must respond to various environmental assaults in a coordinated manner. The endoplasmic reticulum (ER) is a central hub for plant responses to various stresses. We previously showed that Phytophthora utilizes effector PsAvh262-mediated BiP accumulation for suppressing the ER stress-triggered cell death. As a BiP binding partner, Bcl-2-associated athanogene 7 (BAG7) plays a crucial role for the maintenance of unfolded protein response (UPR), however, little is known about the role of BAG7 in plant immunity. In this work, we reveal a double-faced role of BAG7 in plant-Phytophthora interaction, which regulates the ER stress-mediated immunity oppositely in different cellular compartments. In detail, it acts as a susceptibility factor in the ER, but plays a resistant role in the nucleus against Phytophthora. Phytophthora infection signals trigger the ER-to-nucleus translocation of BAG7 the same as abiotic heat stress, however, this process can be prevented by PsAvh262-mediated BiP accumulation. Moreover, the immunoglobulin/albumin-binding domain in PsAvh262 is essential for both pathogen virulence and BiP accumulation. Taken together, our study uncovers the double-faced role of BAG7, and Phytophthora utilizes effector to detain of BAG7 in the ER that acts as a susceptibility factor, thus to advance colonization in planta.
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