Rice is exposed to attacks by the three most destructive pathogens, Magnaporthe oryzae (M. oryzae), Xanthomonas oryzae pv. oryzae (Xoo), and Rhizoctonia solani (R. solani), which cause substantial yield losses and severely threaten food security. To cope with pathogenic infections, rice has evolved diverse molecular mechanisms to respond to a wide range of pathogens. Among these strategies, plant microRNAs (miRNAs), endogenous single-stranded short non-coding RNA molecules, have emerged as promising candidates in coordinating plant–pathogen interactions. MiRNAs can modulate target gene expression at the post-transcriptional level through mRNA cleavage and/or translational inhibition. In rare instances, they also influence gene expression at the transcriptional level through DNA methylation. In recent years, substantial advancements have been achieved in the investigation of microRNA-mediated molecular mechanisms in rice immunity. Therefore, we attempt to summarize the current advances of immune signaling mechanisms in rice–pathogen interactions that are regulated by osa-miRNAs, including their functions and molecular mechanisms. We also focus on recent findings concerning the role of osa-miRNAs that respond to M. oryzae, Xoo, and R. solani, respectively. These insights enhance our understanding of how the mechanisms of osa-miRNAs mediate rice immunity and may facilitate the development of improved strategies for breeding pathogen-resistant rice varieties.

Apple (Malus domestica) is one of the most widely cultivated and consumed fruits worldwide, valued for its rich nutrition and health benefits. Low temperature (LT) significantly limits apple growth, productivity, and fruit quality. Understanding the intricate regulatory networks, underlying cold tolerance is crucial for developing resilient apple cultivars. In this review, we comprehensively summarize the molecular control enabling apple to withstand cold stress, encompassing transcription cascades, phytohormonal networks, reactive oxygen species (ROS) regulation, epigenetic modifications, and post-translational modifications (PTMs), as well as the crosstalk with drought, immune, and light signaling pathways. We also discuss the management strategies for enhancing apple cold tolerance, including the exploitation of wild germplasm resources, multi-omics-based network integration, gene editing, molecular marker-assisted breeding, rootstock grafting, and emerging bioinoculants approaches. This review provides a foundational framework for molecular breeding and gene regulatory strategies to improve cold resilience in apple.

Growing resistant rice cultivars is the most effective strategy to control bacterial blight (BB), a devastating disease caused by Xanthomonas oryzae pv. oryzae (Xoo). Screening resistant germplasm and identifying resistance (R) genes are prerequisites for breeding resistant rice cultivars. We conducted a genome-wide association study (GWAS) to detect quantitative trait loci (QTL) associated with BB resistance using 359 East Asian temperate Japonica accessions inoculated with two Chinese Xoo strains (KS6-6 and GV) and one Philippine Xoo strain (PXO99^A). Based on the 55K SNPs Array dataset of the 359 Japonica accessions, eight QTL were identified on rice chromosomes 1, 2, 4, 10, and 11. Four of the QTL coincided with previously reported QTL, and four were novel loci. Six R genes were localized in the qBBV-11.1, qBBV-11.2, and qBBV-11.3 loci on chromosome 11 in this Japonica collection. Haplotype analysis revealed candidate genes associated with BB resistance in each QTL. Notably, LOC_Os11g47290 in qBBV-11.3, encoding a leucine-rich repeat receptor-like kinase, was a candidate gene associated with resistance to the virulent strain GV. Knockout mutants of Nipponbare with the susceptible haplotype of LOC_Os11g47290 exhibited significantly improved BB resistance. These results will be useful for cloning BB resistance genes and breeding resistant rice cultivars.

Nuclear processes underpin host phenotypic plasticity and environmental adaptation, yet how distinct nuclear processes are coordinated in response to external biotic stimuli remains elusive. Here, we employed genome-wide association study (GWAS) to identify OsTOPBP1C, encoding a multifunctional protein that modulates rice resistance to bacterial blight (BB) caused by Xanthomonas oryzae pv. oryzae (Xoo). We discovered that the Xoo-secreted transcription activator-like effector TalDR22^GIV subverts host immunity by commandeering the transcriptional control of OsTOPBP1C. This effector antagonizes OsTOPBP1C transcription induced jointly by the avirulence protein TalAE73^GIV and the DNA damage response integrator OsSOG1, thereby sustaining DNA repair function and counteracting immune responses. Promoter activity assays and transcriptomic analyses support that OsTOPBP1C fine-tunes rice immunity via a transcription-dependent mechanism. Mechanistically, OsTOPBP1C exerts dual roles in rice immunity: under infection, reduced transcription shifts its function toward DNA repair, which promotes OsSOG1-mediated susceptibility; conversely, high transcription enables it to potentiate salicylic acid (SA)-mediated defense through suppressing OsSAH3 transcription activated by OsMYC2. Our findings reveal a pathogen strategy for rewiring host nuclear processes and demonstrate how host gene transcription shapes immune plasticity, offering insights into the molecular choreography of host-pathogen interactions.