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.

Salicylic acid (SA) plays a crucial regulatory role in plant immunity. NPR1 (non-expressor of pathogenesis related-1) is a SA receptor and plays a pivotal role in SA signaling. However, pathogen effectors which target NPR1 to promote infection have rarely been reported. Here, we identified a Phytophthora capsici effector RxLR48 that associates with NPR1, facilitates P. capsici infection and is required for pathogen virulence. Furthermore, we demonstrated that RxLR48 promotes NPR1's nuclear localization and inhibits its proteasome-mediated degradation, suggesting that RxLR48 suppresses SA signaling by targeting the central regulator NPR1. In addition, we showed that RxLR48 also suppresses pattern-triggered immunity (PTI). Together, our research indicates that P. capsici suppresses plant immunity by targeting SA and PTI pathways.

Due to the monocultural basis of agricultural crops, mutated plant microbes with increased pathogenicity can easily spread in the field and lead to serious yield losses. As a major threat to a wide range of crop plants, oomycete pathogens continuously undergo adaptive evolution to overcome plant defense barriers. However, the genetic basis of their evolution at the molecular level remains largely unknown. Here, we investigated the nature variation and the population genomics of the soybean pathogen Phytophthora sojae by high-throughput genome re-sequencing. Genomic variation analysis revealed uneven “two-speed” evolutionary pattern with genes in gene-sparse regions (GSRs) showing higher rates of structural polymorphisms and positive selection. GSRs are enriched in effector genes and transposase-related genes. Our results also suggested that the NADH oxidase and MIP transporter gene families undergo rapid and diversifying selection. Furthermore, we demonstrated that P. sojae isolates possess varying numbers of RxLR effectors with diverse sequences, totaling 471 members. Among them, 42 core RxLR effectors are assumed to be important for infection. Finally, we observed that Avr genes exhibit abundant sequence variation in P. sojae isolates. Several novel variants lead to the evading of host resistance, including a complete deletion in Avr3c and amino acid mutations in Avr1a. Taken together, our results provide an adaptive landscape of P. sojae at single-nucleotide resolution, as well as resources for further resistance breeding and disease prevention against this important plant pathogen.