Soybean (Glycine max L.) is a vital grain and oil crop, serving as a primary source of edible oil, plant-based protein, and livestock feed. Its production is crucial for ensuring global food security. However, soybean yields are severely impacted by various diseases, and the development of disease-resistant cultivars remains the most sustainable strategy for mitigating these losses. While stable genetic transformation is a common approach for studying gene function, virus-induced gene silencing (VIGS) offers a rapid and powerful alternative for functional genomics, enabling efficient screening of candidate genes. Nevertheless, the application of VIGS in soybean has been relatively limited. In this study, we established a tobacco rattle virus (TRV)-based VIGS system for soybean, utilizing Agrobacterium tumefaciens-mediated infection. The TRV vector was delivered through cotyledon nodes, facilitating systemic spread and effective silencing of endogenous genes. Our results demonstrate that this TRV–VIGS system efficiently silences target genes in soybean, inducing significant phenotypic changes with a silencing efficiency ranging from 65% to 95%. Key genes, including phytoene desaturase (GmPDS), the rust resistance gene GmRpp6907, and the defense-related gene GmRPT4, were successfully silenced, confirming the system’s robustness. This work establishes a highly efficient TRV–VIGS platform for rapid gene function validation in soybean, providing a valuable tool for future genetic and disease resistance research.

The COP9 signalosome (CSN) is a highly conserved eukaryotic protein complex that plays a crucial role in plant growth, development, and stress responses by modulating the ubiquitination pathway. Emerging evidence underscores its significance in plant immunity, where it orchestrates diverse defense mechanisms, including hormone signaling, reactive oxygen species (ROS), homeostasis, and secondary metabolite (SM) biosynthesis. As a key regulator, CSN influences multiple layers of immune responses, such as pattern-triggered immunity (PTI), effector-triggered immunity (ETI), and systemic acquired resistance (SAR). However, the intricate interplay between CSN and immune regulatory networks remains incompletely understood, and a comprehensive model of its mechanistic framework is still lacking. This review systematically consolidates current knowledge on CSN-mediated immune regulation in plant–pathogen interactions and highlights its role in disease resistance.

Stem lodging significantly reduces soybean yield stability, particularly under dense planting and intercropping systems. Stem breaking strength is a key component of lodging resistance, but its genetic basis remains incompletely understood. In this study, an F₂ population consisting of 167 individuals derived from a cross between nanxiadou25 (NXD25, high stem breaking strength) and Shiyuehuang (SYH, low stem breaking strength) was analyzed using bulked segregant analysis with whole-genome resequencing (BSA-Seq) to identify loci associated with stem breaking strength. The trait showed broad quantitative variation in the F₂ population, ranging from 20.1 to 673.7 N. Two extreme bulks were constructed using 30 plants with the highest values and 30 plants with the lowest values. QTL-seq detected 21 candidate intervals at the 95% confidence level, among which, three major loci on Chr07, Chr13, and Chr16 exceeded the 99% threshold and were designated qBR7.2, qBR13.1, and qBR16.1. By integrating large-effect SNP/InDel variation, marker development, RNA-seq profiling, and qRT-PCR validation, nine candidate genes were retained for further study, and three marker-linked genes were highlighted as high-priority candidates. RNA-seq identified 9617 differentially expressed genes between the two parents. In addition, three co-dominant InDel markers, Chr07_01, Chr13_17, and Chr16_83, showed phenotype-consistent polymorphism in extreme F₂ individuals. These findings provide valuable loci, candidate genes, and molecular markers for soybean lodging-resistance breeding.