Bacterial wilt, caused by Ralstonia solanacearum, is one of the most destructive soil-borne diseases a ffecting p epper ( Capsicum annuum L.) production. Developing resistant cultivars is considered the most effective strategy for sustainable disease management. This study investigated the genetic basis of bacterial wilt resistance using an F₂ population derived from a cross between the resistant line ‘FRH1’ a nd t he s uscep tible line ‘ Saengryeok211’. A total o f 180 F ₂ individuals were evaluated for disease response following artificial inoculation with R. solanacearum. Disease severity was assessed using a disease index (DI) scale based on wilting symptoms, and the distribution of DI values showed continuous variation. Classifying individuals with DI 0–1 as resistant and those with DI 2–4 as susceptible, the segregation ratio fit the expected 1:3 ratio, suggesting that resistance may involve a recessive major gene. A genetic linkage map was c onstructed u sing single nucleotide p olymorp hism ( SNP) m arkers d erived from genotyping-by-sequencing (GBS) data. Composite interval mapping subsequently identified a genomic region on chromosome 5 associated with bacterial wilt resistance. This identified Quantitative Trait L ocus ( QTL) e xp lained a s ignificant p rop ortion o f phenotyp ic v ariation a nd o ffers v aluable information for marker-assisted selection in pepper breeding programs.

Interspecific hybridization is a fundamental strategy in ornamental plant breeding, which enables the combination of desirable traits. In Lilium, complex hybrids, including longiflorum-Asiatic (LA) and Oriental-Trumpet (OT) cultivars, have been extensively developed via interspecific crosses between distantly related genome groups. However, the genomic structure and chromosomal behavior of these commercially important hybrids are largely uncharacterized. In this study, we applied genomic in situ hybridization (GISH) to eight triploid LA and OT lily cultivars to evaluate their chromosomal composition, assess their genome stability, and explore the utility of GISH as a practical cultivar verification tool. Flow cytometry and somatic chromosome counting confirmed the triploid status (2n = 3x = 36) of all the assessed cultivars. GISH analysis also revealed distinct parental chromosome sets in the background of each hybrid, with no evidence of intergenomic translocations or recombination. The LA cultivars exhibited 12 chromosomes derived from L. longiflorum and 24 from Asiatic parents, whereas the OT cultivars demonstrated 12 chromosomes of Oriental hybrid origin and 24 derived from Trumpet hybrids. This consistent non-recombinant genomic structure across all the cultivars strongly supports somatic polyploidization as the primary mechanism underlying their development. The suppression of homoeologous recombination underscores the cytogenetic stability of these hybrids and supports their clonal maintenance through vegetative propagation. Furthermore, these findings validate GISH as an effective tool for cultivar verification and chromosomal assessment in ornamental plant breeding and reinforce the importance of cytogenetic profiling for the development and management of interspecific hybrids.

Trigeminal neuralgia is a neuropathic pain disorder characterized by sudden, intense, and recurrent episodes of electric shock-like pain within the distribution of the trigeminal nerve. In addition to pain triggered by normally nonpainful stimuli, it may also present as spontaneous episodes. Although various causes of trigeminal neuralgia have been identified―such as neurovascular compression, demyelination, injury, and tumors―the underlying pathophysiological mechanisms remain poorly understood. Understanding these mechanisms is therefore crucial; however, the animal models used in research do not fully replicate the causes of the disorder. This review provides an overview of the animal models employed in trigeminal neuralgia research and evaluates their suitability for investigating disease mechanisms. Among these models, trigeminal root compression and demyelination models most closely reproduce the clinical etiology of trigeminal neuralgia. Developing animal models that accurately reflect the clinical pathophysiology of trigeminal neuralgia is essential for elucidating the underlying mechanisms and advancing the preclinical evaluation of new pharmacological agents and therapeutic interventions.