The tomato cytoplasmic receptor-like kinase TPK09 mediates resistance to Botrytis cinerea and tolerance to light-induced stress

Regulation of reactive oxygen species production by LrWRKY53 transcription factor promotes leaf senescence and Botrytis cinerea susceptibility in lily.

WRKY transcription factors (TFs) play regulatory roles in leaf senescence and resistance to biotic stress. Elucidation of the underlying regulatory mechanisms is crucial for improving crop performance and resistance. However, functional characterization of WRKY TFs in Lilium species is limited. Here, three Botrytis cinerea-responsive genes, LrWRKY33b, LrWRKY41b, and LrWRKY53, were cloned from L. regale Wilson and transiently expressed in tobacco to investigate the specific role of LrWRKY53 in leaf yellowing. LrWRKY53 is a 308-amino-acid cluster III protein encoded by a 927-bp open reading frame. Tissue-specific analysis showed that LrWRKY53 was significantly upregulated in senescent leaves and was responsive to salicylic acid (SA) and jasmonic acid (JA) signaling. LrWRKY53 was localized to the nucleus and demonstrated transcriptional activity in yeast cells. Transient overexpression of LrWRKY53 in lily plants induced leaf yellowing and increased susceptibility to Botrytis cinerea infection, which was suppressed on downregulation of LrWRKY53. LrWRKY53 overexpression led to significantly increased levels of hydrogen peroxide and the oxygen anion (O2-). Moreover, overexpression of LrWRKY53 in Arabidopsis promoted leaf senescence and enhanced B. cinerea susceptibility, which coincided with increased production of reactive oxygen species (ROS) and upregulation of the associated respiratory burst oxidase homolog (AtRboh)A and AtRbohD genes. Furthermore, yeast one-hybrid and transactivation assays indicated that LrWRKY53 activated the promoter of LrRBOH1 isolated from L. regale. Collectively, this is the first report of a WRKY regulator mediating leaf senescence and B. cinerea susceptibility in lily through its effects on ROS homeostasis.

Integrated transcriptome and metabolome analysis of resistant and susceptible tomato cultivars in response to tomato mottle mosaic virus and functional characterization of snakin-2 in viral defense.

Tomato mottle mosaic virus (ToMMV) is an emerging tobamovirus causing severe losses in tomato production. To elucidate host resistance mechanisms, we compared two tomato cultivars with contrasting responses to ToMMV using integrated transcriptomic, metabolomic, and functional analyses. The resistant line (R) carried resistance gene Tm‑2² at extremely low levels, while the susceptible line (S) did not; both lines highly expressed susceptibility gene tm-2. R plants exhibited minimal viral accumulation and maintained chlorophyll levels, whereas S plants showed high viral load and chlorophyll degradation. Multi-omics revealed that in S, ToMMV primarily disrupted chlorophyll biosynthesis and photosynthesis, while activating multiple defense pathways, including plant-pathogen interaction, phenylpropanoid/flavonoid biosynthesis, and MAPK signaling. In R, a broader activation of plant-pathogen interaction and phosphatidylinositol signaling pathways was observed, alongside early upregulation of SlSN2. The abundance of phenolic acids, notably caffeic acid, ferulic acid, and sinapic acid, was significantly higher in R than in S. Integrated transcriptomic and metabolomic analyses showed that both differential genes and metabolites were co-enriched in the phenylpropanoid biosynthesis pathway. Functional assays demonstrated that SlSN2 overexpression suppressed ToMMV accumulation and infection, likely via enhanced lignin biosynthesis. These findings suggest a potential role for SlSN2 in contributing to ToMMV resistance, independent of the known Tm‑2² pathway. This work identifies SlSN2 as a candidate factor for further evaluation in the prevention of ToMMV.

StLecRK. IX and StLRPK1 form a complex with StBAK1 to positively regulate potato late blight resistance.

In plants, numerous receptor-like kinases (RLKs) function as potential pattern recognition receptors (PRRs) involved in perceiving ligands to trigger pattern-triggered immunity (PTI); however, the roles of most RLKs remain uncharacterized. A previous study showed that the potato receptor-like kinase StLRPK1 interacts with the co-receptor SERK3A/BAK1 to positively regulate resistance against Phytophthora infestans, yet the underlying mechanism remains unknown. Here, we identified StLecRK. IX, a potato RLK that interacts with StLRPK1. The expression of StLecRK. IX was up-regulated in response to P. infestans inoculation. Transient overexpression of StLecRK. IX triggered strong cell death in Nicotiana benthamiana leaves. Moreover, stable overexpression of either StLecRK. IX or its N. benthamiana ortholog NbLecRK. IX significantly enhanced late blight resistance in both potato and N. benthamiana by activating a cascade of immune responses, including reactive oxygen species (ROS) burst, transcriptional upregulation of PTI marker genes, and callose deposition. StLecRK. IX contains two conserved functional motifs, HRD and DFG, within its kinase domain and exhibits strong kinase activity. Furthermore, we demonstrate that StLRPK1 and StLecRK. IX form a ternary protein complex with the co-receptor SERK3A/BAK1 to positively regulate late blight resistance. Together, these findings expand our understanding of plant RLK functions in late blight resistance and provide a strategic basis for utilizing StLecRK. IX and StLRPK1 to improve potato resistance, and highlight StLecRK. IX as a promising target for engineering disease resistance in crops.

Down-regulation of VvPLL3 enhances grapevine resistance to Erysiphe necator via defense activation and cell wall remodeling.

The Small GTPase RHO1 Regulates ROS Homeostasis and Differentially Responds to Pathogens Infection via Interaction With Aquaporin TIP1;1 in Nicotiana

ABSTRACT Small G‐proteins are crucial regulators in plant growth and environmental responses. However, the mechanistic basis underlying their regulation of plant immunity to different pathogens is still poorly understood. Here, we showed that the small GTPase Ras homologous 1 (RHO1) responded differently to infection by distinct pathogens. Overexpression of RHO1 increased the plant susceptibility to chilli veinal mottle virus (ChiVMV) and necrotrophic Botrytis cinerea infections but enhanced plant resistance to the biotrophic bacterium Pseudomonas syringae . Further exploration revealed that there existed a direct interaction between RHO1 and tonoplast intrinsic protein 1;1 (TIP1;1), an aquaporin involved in water movement and the transport of hydrogen peroxide (H2O2) between vacuoles and cytoplasm. Under pathogen infection, the interaction between RHO1 and TIP1;1 could affect the distribution of reactive oxygen species (ROS) in the cytoplasm and vacuoles, promote the accumulation of ROS in the cytoplasm, leading to different responses of plant cells to pathogens with different lifestyles. Furthermore, the expression level of TIP1;1 was altered under infection by different pathogens. Our results demonstrate a mechanism by which the small GTPase RHO1 regulates ROS compartmentalization to affect the plant response to different pathogen infections, indicating the diversity of responses of a plant gene to different biotic factors.

An AAA+ ATPase–F-box module regulates potato late blight resistance by affecting SOBIR1 stability

Fine-tuning immune receptor stability is essential for maintaining the balance between defense and growth in crops. Here, we identify an AAA+ ATPase–F-box regulatory module that negatively regulates potato immunity by promoting the degradation of the immune co-receptor StSOBIR1. The AAA+ ATPase StGCN4 functions as a negative regulator of potato immunity. Silencing of StGCN4 markedly enhanced resistance to Phytophthora infestans without affecting plant growth, while overexpression increased susceptibility. StGCN4 interacts with the PP2-type F-box protein StPFB1 and stabilizes it at the plasma membrane, which also negatively regulate immunity and together they facilitate proteasomal degradation of StSOBIR1, thereby dampening receptor-mediated defense signaling. Suppression of StGCN4 or StPFB1 enhances reactive oxygen species (ROS) production, salicylic acid accumulation, and expression of defense-related genes, resulting in strong resistance to P. infestans without growth penalty. These findings reveal a previously unrecognized AAA+ ATPase–F-box module that controls receptor homeostasis and identify StGCN4 as a promising molecular target for breeding high-yielding and late blight resistant potato cultivars.