Peanut (Arachis hypogaea), a globally important oilseed crop, exhibits contrasting growth habits between wild species (prostrate) and cultivated varieties (erect or spreading), but the underlying mechanism is unclear. In this study, we performed quantitative trait locus (QTL) mapping of two recombinant inbred line (RIL) populations of peanut using SNP arrays and bulk segregant analysis, which identified qGH15 on chromosome 15 as a major QTL regulating growth habit. Fine mapping using KASP markers narrowed the candidate region to a 151-kb interval, while analysis of a residual heterozygous line (RHL) further delimited qGH15 to a 38-kb interval containing a single candidate gene, which we designated as AhGH15. Genotyping of a natural population revealed multiple types of polymorphisms in this gene associated with the erect habit in cultivated varieties. Phylogenetic and pedigree analyses demonstrated that these polymorphisms were recurrently and convergently selected during peanut domestication and breeding, with modern hybridization accelerating their dissemination. Transcriptome deep sequencing and gene co-expression analysis via WGCNA revealed polymorphism-specific patterns of transcriptome regulation, with co-expressed gene modules differentially active between accessions with erect or prostrate growth habits. These findings establish AhGH15 as a key determinant of peanut growth habit and highlight its complex selection history during peanut improvement.

Late leaf spot disease (LLS) is one of the most important diseases that cause severe yield losses in peanut. Peanut has various sources of resistance to LLS, so the identification of resistant quantitative trait loci (QTLs) and the development of related molecular markers are of great importance for the breeding of LLS-resistant peanut. In this study, 173 individual lines of a recombinant inbred line (RIL) population and the 48K SNP array for genotyping were used to construct a high-density genetic map with 1,475 bin markers and 20 linkage groups. A total of 11 QTLs were obtained through QTL analysis using the constructed genetic map. Among them, the stable major QTL qLLS.LG02 was identified on linkage group 2 in all six environments, with the phenotypic variation explained (PVE) ranging from 15.57 to 31.09%. QTL-seq technology was also employed for a QTL analysis of LLS resistance. As a result, 14 QTL loci related to LLS resistance were identified using the G prime algorithm. Notably, the physical positions of qLLS02 and qLLS03 coincided with those of qLLS.LG02 and qLLS.LG03, respectively. Gene annotation analysis within the 14 QTL intervals from QTL-seq revealed a total of 163 nucleotide-binding site–leucine-rich repeat (NBS-LRR) disease resistance genes, accounting for 22.86% of all resistance (R) genes in the peanut genome and showing a 4.26-fold enrichment with a P-value of 5.19e–57. Within the QTL region qLLS02 of the resistant parent Mi-2, there was a 5 Mb structural variation (SV) interval containing 81 NBS-LRR genes. A PCR diagnostic marker was developed, and validation data suggested that this SV might lead to gene deletion or replacement with other genes. This SV has the potential to enhance peanut resistance to LLS. The results of this study have significant implications for improving peanut breeding for LLS resistance through the development of associated molecular markers.