Peanut stem rot, also known as white mold, poses a significant threat to peanut production. It is typically managed using fungicides and moderately resistant cultivars. Cultivars with higher resistance can reduce fungicide dependency and increase sustainability. This study explores the potential of wild peanut species in stem rot resistance breeding programs by enhancing genetic diversity in cultivated peanut. Through greenhouse and field evaluations, 13 allotetraploid hybrids with Arachis stenosperma as one of the parents showed superior resistance compared to other wild genotypes. The genomic regions that confer the stem rot resistance were further identified by genotyping and phenotyping an F₂ population derived from the allotetraploid ValSten1 (A. valida × A. stenosperma)^4× and A. hypogaea cv. TifGP-2. A linkage map was constructed from 1926 SNP markers. QTL analysis revealed both beneficial and deleterious loci, with two resistance-associated QTLs derived from A. stenosperma and four susceptibility loci, two from A. stenosperma and two from A. valida. This is the first study that evaluated peanut-compatible wild-derived allotetraploids for stem rot resistance and that identified wild-derived QTLs for resistance to this pathogen. The allotetraploid hybrid ValSten1, that has A. stenosperma as one of the parents, offers a resource for resistance breeding. Markers associated with resistance QTLs can facilitate introgression from ValSten1 into cultivated peanut varieties in future breeding efforts, potentially reducing reliance on chemical control measures.

The allotetraploid legume peanut ( Arachis hypogaea L.) has low genetic diversity due to the single origin and ploidy barrier with its wild relatives, which are mostly diploid. This lack of genetic diversity hinders breeding and genetic gains. Wild peanut relatives harbor known resistances to pests and diseases and genetic variation that can contribute to adaptation to diverse environments and a changing climate. The ploidy barrier between the wild relatives and the cultigen can be surpassed by the production of induced allotetraploids using parents with genomes that are compatible to those of peanut. Here, we crossed seven accessions of six Arachis species. All combinations carried at least one of the peanut progenitors, A. ipaënsis and A. duranensis , crossed with a species of complementary genome. The original hybrids were treated with colchicine for recovery of fertility, observed by pollen viability and seed production. Six new allotetraploids were produced; they were named WPL‐BatDur1 (Reg. no. GP‐248, PI 707934), WPL‐BatDur2 (Reg. no. GP‐249, PI 707936), WPL‐MagDur1 (Reg. no. GP‐253, PI 707942), WPL‐IpaCor1 (Reg. no. GP‐251, PI 707938), WPL‐IpaDur1 (Reg. no. GP‐250, PI 707937), and WPL‐IpaVillo1 (Reg. no. GP‐252, PI 707941), released by the University of Georgia. Cytogenetic analyses confirmed the tetraploid plants had 20 A‐type and 20 B‐ or K‐type chromosomes. All these allotetraploids have surprisingly high protein content. They also show moderate to strong resistance to the main peanut fungal diseases (late and early leaf spot and rust) and Southern stem rot, are compatible with cultivated peanut, and are being used in breeding programs in the United States, Senegal, and Brazil for the development of resilient peanut cultivars.

Bacterial soft rot, caused by Pectobacterium carotovorum subsp. carotovorum, affects numerous vegetable crops. Beneficial microbes like Bacillus amyloliquefaciens PMB05 offer a sustainable alternative to traditional copper- or antibiotic-based controls, which risks the development of pathogen resistance. Bacillus amyloliquefaciens PMB05 enhances disease resistance to soft rot by intensifying PAMP-triggered immunity (PTI). Although our previous research showed that PMB05-intensified PTI correlates with a reduced photosynthetic electron transport rate under high light conditions, it remains unclear whether increasing light intensity can strengthen PMB05-mediated immune signaling to further enhance disease resistance in plant leaves. In this study, Arabidopsis plants were grown under varying light intensities to address this question. Furthermore, expression of the type III elicitor, HrpN protein, was applied to evaluate the impact of PMB05 treatment on immune activation. HrpN acts as a PAMP that can trigger plant defense responses. The results revealed that higher growth light intensity was associated with PMB05-intensified PTI response by increasing reactive oxygen species generation but suppresses callose deposition. In addition, PMB05-facilitated PTI-mediated stomatal closure occurred more rapidly and tightly under high light, thereby restricting pathogen invasion into leaf tissues. Disease assays further confirmed that higher light intensity significantly reduced soft rot severity in A. thaliana, while the combination of high light and PMB05 treatment achieved superior control efficacy. Furthermore, PMB05-associated disease protection under high growth light was not detected in sid2, npr1, and nahG plants, indicating that intact SA-associated functions are required for the detectable protective phenotype under the conditions tested. These findings demonstrate that environmental light management can strategically potentiate immunity-intensifying microbes, establishing a novel paradigm for sustainable disease control through the coordinated manipulation of light conditions and microbial application.