Plants rely on multiple immune systems to protect themselves from pathogens. When pattern-triggered immunity (PTI)—the first layer of the immune response—is no longer effective as a result of pathogenic effectors, effector-triggered immunity (ETI) often provides resistance. In ETI, host plants directly or indirectly perceive pathogen effectors via resistance proteins and launch a more robust and rapid defense response. Resistance proteins are typically found in the form of nucleotide-binding and leucine-rich-repeat-containing receptors (NLRs). Upon effector recognition, an NLR undergoes structural change and associates with other NLRs. The dimerization or oligomerization of NLRs signals to downstream components, activates “helper” NLRs, and culminates in the ETI response. Originally, PTI was thought to contribute little to ETI. However, most recent studies revealed crosstalk and cooperation between ETI and PTI. Here, we summarize recent advancements in our understanding of the ETI response and its components, as well as how these components cooperate in the innate immune signaling pathways. Based on up-to-date accumulated knowledge, this review provides our current perspective of potential engineering strategies for crop protection.

The specialized plasma membrane microdomains known as lipid rafts are enriched by sterols and sphingolipids. Lipid rafts facilitate cellular signal transduction by controlling the assembly of signaling molecules and membrane protein trafficking. Another specialized compartment of plant cells, the plasmodesmata (PD), which regulates the symplasmic intercellular movement of certain molecules between adjacent cells, also contains a phospholipid bilayer membrane. The dynamic permeability of plasmodesmata (PDs) is highly controlled by plasmodesmata callose (PDC), which is synthesized by callose synthases (CalS) and degraded by β-1,3-glucanases (BGs). In recent studies, remarkable observations regarding the correlation between lipid raft formation and symplasmic intracellular trafficking have been reported, and the PDC has been suggested to be the regulator of the size exclusion limit of PDs. It has been suggested that the alteration of lipid raft substances impairs PDC homeostasis, subsequently affecting PD functions. In this review, we discuss the substantial role of membrane lipid rafts in PDC homeostasis and provide avenues for understanding the fundamental behavior of the lipid raft–processed PDC.

Arabidopsis glucosyl sphingolipid-modulated plasmodesmal gating involves modulation of the glycosylphosphatidylinositol-anchored PdBG2 protein secretion machine

Pathogens generate and secrete effector proteins to the host plant cells during pathogenesis to promote virulence and colonization. If the plant carries resistance (R) proteins that recognize pathogen effectors, effector‐triggered immunity (ETI) is activated, resulting in a robust immune response and hypersensitive response (HR). The bipartite effector AvrRps4 from Pseudomonas syringae pv. pisi has been well studied in terms of avirulence function. In planta, AvrRps4 is processed into two parts. The C‐terminal fragment of AvrRps4 (AvrRps4^C) induces HR in turnip and is recognized by the paired resistance proteins AtRRS1/AtRPS4 in Arabidopsis. Here, we show that AvrRps4^C targets a group of Arabidopsis WRKY, including WRKY46, WRKY53, WRKY54, and WRKY70, to induce its virulence function. Indeed, AvrRps4^C suppresses the general binding and transcriptional activities of immune‐positive regulator WRKY54 and WRKY54‐mediated resistance. AvrRps4^C interferes with WRKY54's binding activity to target gene SARD1 in vitro, suggesting WRKY54 is sequestered from the SARD1 promoter by AvrRps4^C. Through the interaction of AvrRps4^C with four WRKYs, AvrRps4 enhances the formation of homo‐/heterotypic complexes of four WRKYs and sequesters them in the cytoplasm, thus inhibiting their function in plant immunity. Together, our results provide a detailed virulence mechanism of AvrRps4 through its C‐terminus.

Plant resistance proteins recognize cognate pathogen avirulence proteins (also named effectors) to implement the innate immune responses called effector-triggered immunity. Previously, we reported that hopA1 from Pseudomonas syringae pv. syringae strain 61 was identified as an avr gene for Arabidopsis thaliana. Using a forward genetic screen approach, we cloned a hopA1-specific TIR-NBS-LRR class disease resistance gene, RESISTANCE TO PSEUDOMONAS SYRINGAE6 (RPS6). Many resistance proteins indirectly recognize effectors, and RPS6 is thought to interact with HopA1_Pss61 indirectly by surveillance of an effector target. However, the involved target protein is currently unknown. Here, we show RPS6 is the only R protein that recognizes HopA1_Pss61 in Arabidopsis wild-type Col-0 accession. Both RPS6 and HopA1_Pss61 are co-localized to the nucleus and cytoplasm. HopA1_Pss61 is also distributed in plasma membrane and plasmodesmata. Interestingly, nuclear localization of HopA1_Pss61 is required to induce cell death as NES-HopA1_Pss61 suppresses the level of cell death in Nicotiana benthamiana. In addition, in planta expression of hopA1_Pss61 led to defense responses, such as a dwarf morphology, a cell death response, inhibition of bacterial growth, and increased accumulation of defense marker proteins in transgenic Arabidopsis. Functional characterization of HopA1_Pss61 and RPS6 will provide an important piece of the ETI puzzle.

Transcription factors (TFs) function as master regulators in multiple signaling pathways and govern diverse developmental and adaptive processes in plants. Some TFs identified in crop plants play critical roles in regulating yield through changes in plant architecture, including roots, stems, leaves, flowers, fruits, and grains. Although altering crop architecture can increase yields, the extent of yield enhancement is frequently hampered by diseases. Developing new crop varieties with improved yields and enhanced disease resistance remains challenging because immune system activation often impairs plant growth. Recently, approaches using TF engineering have made substantial progress in elevating both growth performance and disease resistance. However, most of these techniques rely on traditional transgenic methods. This review highlights discoveries in the last decade demonstrating improvements in growth performance, yield and immunity through TF engineering. We focus mainly on changes in plant architecture related to improved yield and disease resistance. We conclude with perspectives on the potential application of these discoveries for generating desirable crop traits by merging the most noteworthy biotechnology approaches, such as clustered regularly interspaced small palindromic repeats (CRISPR)/CRISPR‐associated protein 9‐mediated genome editing, with canonical molecular biology.