Wild peanut (Arachis) species are promising sources of disease resistance for improving peanut cultivars. The objective of this study was to assess cross-compatibility among cultivated and wild peanuts in crosses between eight peanut cultivars and 27 wild species carrying the A, B, E, Ex, F, K, P, and H genomes. Embryo culture and chromosome doubling led to polyploids representing hybrids between cultivated peanut and A. stenosperma, A. macedoi, A. duranensis, A. villosa, and A. diogoi. The first two showed greater resistance to bacterial wilt than their cultivated parents. DNA markers were developed for verifying the hybrids and for identifying translocation or introgression lines with alien chromosome fragments.

The pathogenesis-related protein PR10 plays a vital role in plant growth, development, and stress responses. This study systematically identified and analyzed PR10 genes in cultivated peanut (Arachis hypogaea L.), examining their phylogenetic relationships, conserved motifs, gene structures, and syntenic relationships. The analysis identified 54 AhPR10 genes, which were classified into eight groups based on phylogenetic relationships, supported by gene structure and conserved motif characterization. Analysis of chromosomal distribution and synteny demonstrated that segmental duplications played a crucial role in the expansion of the AhPR10 gene family. The identified AhPR10 genes exhibited both constitutive and inducible expression patterns. Significantly, AhPR10-7, AhPR10-33, and AhPR10-41 demonstrated potential importance in peanut resistance to Aspergillus flavus. In vitro fungistatic experiments demonstrated that recombinant AhPR10-33 effectively inhibited A. flavus mycelial growth. These findings provide valuable insights for future investigations into AhPR10 functions in protecting peanut from A. flavus infection.

Fresh-seed germination (FSG) impairs peanut production, especially in areas where the peanut harvest season coincides with rainy weather. Developing FSG-resistant cultivars by molecular breeding is expected to mitigate yield loss and quality impairment caused by FSG. However, the genetic control of FSG awaits elucidation. In this study, FSG at 1, 3, 5, 7, and 9 days post-imbibition in three environments were tested, and quantitative-trait loci (QTL) associated with FSG were mapped in a peanut recombinant inbred line population by leveraging existing high-densitypeanut geneticmaps. Of 24 QTL identified in 13 linkage groups, qFSGA04 was a stable major QTL on linkage group 04 (LG04). It was consistently detected in five germination stages and three environments. By designing and validating DNA markers in the confidence interval of qFSGA04, we identified one single-nucleotide polymorphism and one InDel closely associated with FSG that could be used as linked markers for FSG resistance in peanut breeding.