The wheat blast fungus Magnaporthe oryzae pathotype Triticum (MoT) poses a severe threat to global wheat (Triticum aestivum L.) production, yet the molecular mechanisms underlying tissue invasion remain poorly understood.

We performed dual RNA-seq analysis of MoT-inoculated wheat leaves at 0, 24, 36, and 48 hpi, mapping reads separately to the wheat and M. oryzae genomes to capture stage-specific host responses and pathogen gene expression across progressive infection stages.

Wheat exhibited pronounced stage-specific transcriptional reprogramming, with peak differential gene expression at 36 hpi and visible symptoms at 48 hpi. The 24 hpi stage was characterized by rapid induction of immune- and defense-related pathways, including innate immunity and detoxification processes, along with downregulation of cell wall and membrane biosynthesis. By 36 hpi, wheat maintained sustained activation of immune and detoxification pathways, while chloroplast- and photosynthesis-associated genes were broadly repressed, consistent with transcriptional features of metabolic constraint. At 48 hpi, coinciding with lesion initiation, transcriptomes showed persistent, metabolically costly immune and defense responses together with extensive suppression of photosynthesis- and chloroplast-associated functions, which were associated with metabolic strain and a transition toward necrosis. Analysis of pathogen-derived reads revealed temporal induction of multiple effector candidates, including known M. oryzae orthologs and additional effector-like proteins, highlighting coordinated temporal patterns between host immune and metabolic response as well as stage-specific pathogen effector expression.

Together, these findings provide a temporal framework for wheat blast susceptibility and highlight key host pathways and effector candidates that define critical windows for functional dissection of MoT virulence and wheat susceptibility.

Photoperiodism, a seasonal response mechanism that relies on day-length measurement by the circadian clock, is a major regulator of flowering time (Imaizumi 2025). The external coincidence model proposes that the alignment between the internal circadian phase and external light signals triggers photoperiodic responses (Pittendrigh and Minis 1964). It has been challenging to establish robust models for the quantitative relationship between clock and flowering time, due to a lack of tools to modulate the clock quantitatively. Here, using a circadian period-lengthening small molecule, we demonstrated the quantitative modulation of the critical day-length for flowering in monocots.

Transposon silencing via RNA-directed DNA methylation (RdDM) is mediated primarily through 24-nucleotide (nt) small interfering RNAs (siRNAs) and two plant-specific RNA polymerases, Pol IV and Pol V. We generated and characterized RNA-interference (RNAi) lines targeting the largest subunit of Pol IV and Pol V and the second-largest subunit shared by Pol IV and Pol V in soybean. Our analyses showed that the canonical roles of Pol IV and Pol V in RdDM as described in Arabidopsis, whereby Pol IV produces 24-nt siRNAs and Pol V recruits siRNAs to homologous loci to trigger DNA methylation, are conserved in soybean. Our analyses also uncovered functions of Pol IV and Pol V in that they repress defense response genes en masse. These genes normally undergo RdDM and are silenced, but they are de-repressed when Pol IV and Pol V are knocked down. Furthermore, the de-repression of a set of defense-related genes channeled their RNAs into the RNAi pathway to produce 21-22-nt siRNAs. Knocking down Pol IV and Pol V either singly or together led to increased resistance against the oomycete pathogen Phytophthora sojae, suggesting that Pol IV- and Pol V-mediated gene silencing regulates plant immunity.

Herbivorous insects can shape the epidemiology of disease in plants by vectoring numerous phytopathogens. While the consequences of infection are often well-characterized in the host plant, the extent to which phytopathogens alter the physiology and development of their insect vectors remains poorly understood. In this review, we highlight how insect-borne phytopathogens can promote vector fitness, consistent with theoretical predictions that selection should favor a mutualistic or commensal phenotype. In doing so, we define the metabolic features predisposing plant pathogens to engage in beneficial partnerships with herbivorous insects and how these mutualisms promote the microbe's propagation to uninfected plants. For the vector, the benefits of co-opting microbial pathways and metabolites can be immense: from balancing a nutritionally deficient diet and unlocking a novel ecological niche to upgrading its defensive biochemistry against natural enemies. Given the independent origins of these tripartite interactions and a number of convergent features, we also discuss the evolutionary and genomic signatures underlying microbial adaptation to its dual lifestyle as both a plant pathogen and an insect mutualist. Finally, as host association can constrain the metabolic potential of microbes over evolutionary time, we outline the stability of these interactions and how they impact the virulence and transmission of plant pathogens.

Extracellular vesicles (EVs) transport biologically active molecules and are known to mediate host defence against microbial pathogens, including plant fungal pathogens. However, the mechanism by which pathogens disrupt EV-dependent defence remains unclear. Here we show that Phytophthora capsici, a global crop pathogen, counteracts EV-mediated plant defence through targeted lipase activity. We show that Arabidopsis releases EVs containing tetraspanin (TET), specifically TET8- and TET9-EVs, which damage germinated spores of Phytophthora, reducing infection. As a counter-defence, Phytophthora secretes an infection-induced apoplastic lipase, Plant Extracellular Vesicle Destroyer 1 (PED1), which targets TET8- and TET9-EVs. This occurs via interaction with the EV membrane-localized protein Defective Glycosylation 1 (DGL1), which directly interacts and co-localizes with TET8 and TET9 on the EV membrane. PED1 damages TET8- and TET9-EVs through its lipase activity towards campesteryl esters, suppressing EV-mediated plant defence. Our study reveals a mechanism used by Phytophthora to counteract EV-mediated host defence. Phytophthora secretes an infection-induced apoplastic lipase, damaging Arabidopsis extracellular vesicles and suppressing plant defence against infection.

The wheat resistance gene Pm4 encodes a kinase fusion protein and has gained particular attention as it confers race-specific resistance against two major wheat pathogens: powdery mildew and blast. Here we describe the identification of AvrPm4, the mildew avirulence effector recognized by Pm4, using UV mutagenesis, and its functional validation in wheat protoplasts. We show that AvrPm4 directly interacts with and is phosphorylated by Pm4. Using genetic association and quantitative trait locus mapping, we further demonstrate that the evasion of Pm4 resistance by virulent mildew isolates relies on a second fungal component, SvrPm4, which suppresses AvrPm4-induced cell death. Surprisingly, SvrPm4 was previously described as AvrPm1a. We show that SvrPm4, but not its inactive variant svrPm4, is recognized by the nucleotide-binding leucine-rich repeat immune receptor Pm1a. These multiple roles of a single effector provide a new perspective on fungal (a)virulence proteins and their combinatorial interactions with different types of immune receptors. AvrPm4 is a chimeric powdery mildew effector that is recognized by the wheat kinase fusion resistance protein Pm4. The pathogen can evade Pm4 recognition by expressing the suppressor SvrPm4, an RNase-like effector with multiple roles.

Plant cell surface pattern recognition receptors (PRRs) perceive non- or altered-self elicitors to induce immune responses. PRRs relay information across the plasma membrane and trigger downstream signalling via receptor-like cytoplasmic kinases such as BOTRYTIS-INDUCED KINASE 1 (BIK1). BIK1 associates with several PRRs and acts as a key executor of immune responses through the phosphorylation of substrate proteins. However, a comprehensive understanding of how BIK1 targets specific substrates and a full repertoire of these substrates are lacking. Here we defined the substrate specificity of BIK1 and used these data to predict candidate substrates in Arabidopsis. Using high-throughput biochemical and genetic screening of these candidates, we confirmed many as direct BIK1 substrates in vitro and novel regulators of plant immunity. Among the BIK1 substrates identified are MULTIPLE C2 DOMAIN AND TRANSMEMBRANE REGION PROTEIN 3, which we reveal regulates flagellin 22 (flg22)-induced plasmodesmata closure and immunity, and members of the largely uncharacterized CYCLIN-DEPENDENT KINASE-LIKE family, which we uncover as novel negative regulators of immunity. In parallel, we interrogated intracellular NUCLEOTIDE-BINDING LEUCINE-RICH REPEAT (NLR) immune receptors for potential BIK1 phosphorylation motifs and identified multiple NLRs as direct BIK1 substrates. We reveal that BIK1 phosphorylation regulates NLR oligomerization, thus controlling a key activation step for these immune receptors. Together, our unbiased biochemical screens shed light on the central role of BIK1 as a key kinase shaping multiple layers of plant immune signalling. Cell surface receptors perceive immunogenic elicitors, triggering downstream signalling via receptor-like cytoplasmic kinases such as BIK1. Here the authors define and use the phosphorylation motif of BIK1 to find novel substrate candidates.