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

The TaLYK5-TaDSK2a module serves as a molecular switch between plant growth and immunity during fungal attack.

It is demonstrated that the TaLYK5-TaDSK2a module functions as a molecular switch that dynamically regulates the trade-off between plant immunity and growth.

A Phytophthora effector hijacks host StKNOX3‐StHUB1/2 complex to reprogram defense gene expression via histone monoubiquitination

SUMMARY KNOX (KNOTTED1‐like HOMEOBOX) transcription factors regulate the expression of genes involved in plant growth, development, and immunity by specifically binding to DNA elements. Previously, we found that the Phytophthora infestans RxLR effector Pi22798 targets the potato transcription factor StKNOX3 to promote colonization. We show here that StKNOX3 interacts with StHUB1 and StHUB2, two E3 ubiquitin ligases that monoubiquitinate histone 2B to form H2Bub1. StKNOX3 stabilizes StHUB1 and StHUB2 in the nucleus, and the StKNOX3‐StHUB1/2 complex acts to enhance P. infestans infection. The effector Pi22798 promotes the formation of the StKNOX3‐StHUB1/2 complex, facilitating the nuclear accumulation of StHUB1/2, thereby elevating H2Bub1 levels and increasing plant susceptibility. Combined ChIP‐Seq and RNA‐Seq analyses demonstrate that StKNOX3 modulates transcriptome reprogramming governing cell wall composition, phytohormone responses, and stress responses. StKNOX3 directly binds to the core motifs TGAC or TGTCA in promoter regions of target genes and represses the expression of multiple defense‐related genes. Expression of Pi22798 results in reinforced regulation of the StKNOX3‐targeted genes by affecting the binding affinity of StKNOX3 to their promoters and increasing H2Bub1 levels. Our data support a model in which the host StKNOX3‐StHUB1/2 complex is hijacked by Pi22798 to induce epigenetic modifications that ultimately enhance potato susceptibility to P. infestans.

The StABI5-StCAT1 Module Regulates Potato Resistance to Early Blight Through the ROS Signaling Pathway

Simple Summary Potato early blight caused by Alternaria solani poses a serious threat to potato yield and quality. Catalase regulates plant immunity against necrotrophic pathogens, yet its function in early blight remains unclear. In this study, A. solani infection induces hydrogen peroxide accumulation in plants, and exogenous H2O2 application markedly accelerates early blight infection. Furthermore, we identified StCAT1 as a positive regulator of resistance to early blight in potato, with its expression significantly upregulated following A. solani induction. Silencing StCAT1 impaired antioxidant capacity and disease resistance, while overexpression exerted the opposite effect. Additionally, StABI5 was identified as an upstream transcription factor that activates StCAT1 expression, and silencing StABI5 compromised potato resistance to early blight. These results indicate that StABI5 can activate the expression of StCAT1 and by mediating the reactive oxygen species (ROS) signaling pathway regulates potato resistance to early blight, which provides a theoretical basis and genetic resources for the molecular breeding of potato resistance to early blight.

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

Abstract Plant responses to pathogens often rely on receptor-like cytoplasmic kinases (RLCKs) that mediate signaling through interactions with receptor kinases and downstream components. Here, we studied the tomato RLCK, TPK1b Related Protein Kinase (TPK09), and demonstrate its function in integrating defense with light stress responses. Tomato tpk09 mutants exhibited increased susceptibility to Botrytis cinerea and the vascular pathogen Fusarium oxysporum, whereas transgenic expression of TPK09 enhanced resistance to Botrytis. Disease severity in tpk09 mutants was elevated under light-emitting diode (LED) compared to fluorescent light (FL). In the absence of infection, mutants displayed severe necrosis and elevated H2O2 accumulation under LED lighting. TPK09 interacts with the cell death–inducing transglycosylase BcCrh1 from Botrytis. Consistently, TPK09 suppresses cell death triggered by Botrytis infection as well as by BcCrh1 expression. Loss of TPK09 abolished pathogen-induced expression of the tomato suppressor of cell death BAX INHIBITOR-LIKE1 and compromised chitin- and flg22-triggered reactive oxygen species (ROS) accumulation and immune gene activation. Further, TPK09 mitigates damage to the photosynthetic system under elevated light stress, demonstrated by a decrease in the effective photochemical quantum yield of PSII and electron transport rate in the mutant plants. In addition, TPK09 expression is induced by light but suppressed under dark conditions, and the mutant seedlings were insensitive to hypocotyl growth responses to light. RNA sequencing (RNA-seq) studies suggest TPK09 is required for expression of genes involved in light harvesting, photosynthesis, and stress response functions. Collectively, TPK09 plays a key role in enhancing fungal resistance, maintaining the homeostasis of the photosynthetic apparatus and ROS levels, and mitigating photooxidative damage.

Pto evolved from malectin-like RLKs phosphorylates AvrPtoB to promote Prf-mediated immunity in Solanum pimpinellifolium

Gene editing of the transmembrane kinase SOAK1 fine-tunes reactive oxygen species production for enhanced disease resistance in potato.

An RLCK-V subfamily member in potato is reported, StSOAK1, which negatively regulates disease resistance to the oomycete Phytophthora infestans and the fungus Botrytis cinerea and reveals a regulatory mechanism of potato StRBOHB, which occurs in parallel with its paradigmatic AtPBL13-mediated regulation in Arabidopsis.