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Jin-Cheol Kim

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Open access Aug 2026

Characterization of Streptomyces virginiae JCK-8401 for the Suppression of Tomato Bacterial Wilt.

Bacterial wilt caused by Ralstonia solanacearum is a destructive soil-borne disease affecting numerous crops worldwide. Although synthetic pesticides and antibiotics are commonly used for disease management, their excessive application has raised concerns regarding environmental pollution, human health risks, and the emergence of antibiotic-resistant pathogens. As a sustainable alternative, rhizosphere microorganisms have gained attention as potential biocontrol agents. In our previous study, strain JCK-8401 exhibited strong antibacterial activity against R. solanacearum. In the present study, its biocontrol potential was comprehensively characterized through analyses of physiological and biochemical traits, antagonistic activity against phytopathogens, induction of salicylic acid (SA)-mediated defense responses using Arabidopsis thaliana PR1::GUS reporter line, and in vivo suppression of tomato bacterial wilt. Based on 16S rRNA sequence analysis, JCK-8401 was identified as Streptomyces virginiae. The strain utilized diverse carbon sources and produced hydrolytic enzymes and indole-3-acetic acid. Furthermore, it exhibited antibacterial activity against various phytopathogenic bacteria and oomycetes, though it lacked antifungal activity. Both cell suspension and culture filtrate of the strain induced GUS expression, indicating activation of the SA-mediated defense pathway. In vivo assay demonstrated that seed treatment with JCK-8401 achieved 96.40% control efficacy against tomato bacterial wilt. Additionally, pretreatment with diluted culture filtrates (250-, 500-, and 1000-fold) effectively suppressed disease incidence regardless of the application method, strongly suggesting the activation of induced systemic resistance. Overall, Streptomyces virginiae JCK-8401 is a highly promising, multifunctional biocontrol agent for managing soil-borne diseases through a synergistic combination of antibiosis, bioinoculation, and the induction of host plant defense responses.

L. T. Nguyen, A. Park, H. Le et al. · 0 citations
Open access Jul 2026

Development of KASP marker to enhance breeding efficiency for phytophthora blight resistance in sesame through QTL analysis.

BACKGROUND Phytophthora blight, caused by Phytophthora nicotianae, is a destructive disease that severely affects sesame (Sesamum indicum L.). Developing resistant cultivars remains the most effective management strategy. This study aimed to identify genomic regions associated with Phytophthora blight resistance and to develop molecular markers for use in sesame breeding. RESULTS Whole-genome resequencing (WGS) was performed for the resistant cultivar Geonbaek, the susceptible cultivar Milsung, and 99 recombinant inbred lines (RILs). Using a high-density genetic map, we identified a major resistance locus on chromosome 10, designated qPB10. The IM-ADD analysis defined a 0.51-Mb marker interval with an LOD score of 25.67, and a complementary binary-trait analysis independently detected the same locus at 75.10 cM. Genomic analysis of the target region revealed several immune-related genes, including clusters encoding nucleotide-binding leucine-rich repeat (NLR) proteins and other defense-associated factors. To utilize these findings in breeding, kompetitive allele-specific PCR (KASP) markers were developed based on sequence polymorphisms within the qPB10 interval. Validation using the RIL population and a diverse panel of sesame cultivars identified a robust marker that reliably discriminates resistant genotypes. CONCLUSION These findings establish qPB10 as the primary locus governing Phytophthora blight resistance in sesame. The KASP markers developed in this study enable efficient marker-assisted selection without the need for extensive disease phenotyping. These results provide a practical genomic resource for accelerated breeding of resistant cultivars and establish a foundation for future functional characterization of resistance mechanisms.

Jeongeun Lee, Eunyoung Oh, Sungup Kim et al. · 0 citations