Genetic mapping and QTL analysis for peanut smut resistance.

BACKGROUND: Peanut smut is a disease caused by the fungus Thecaphora frezii Carranza & Lindquist to which most commercial cultivars in South America are highly susceptible. It is responsible for severely decreased yield and no effective chemical treatment is available to date. However, smut resistance has been identified in wild Arachis species and further transferred to peanut elite cultivars. To identify the genome regions conferring smut resistance within a tetraploid genetic background, this study evaluated a RIL population {susceptible Arachis hypogaea subsp. hypogaea (JS17304-7-B) × resistant synthetic amphidiploid (JS1806) [A. correntina (K 11905) × A. cardenasii (KSSc 36015)] × A. batizocoi (K 9484)4×} segregating for the trait. RESULTS: A SNP based genetic map arranged into 21 linkage groups belonging to the 20 peanut chromosomes was constructed with 1819 markers, spanning a genetic distance of 2531.81 cM. Two consistent quantitative trait loci (QTLs) were identified qSmIA08 and qSmIA02/B02, located on chromosome A08 and A02/B02, respectively. The QTL qSmIA08 at 15.20 cM/5.03 Mbp explained 17.53% of the phenotypic variance, while qSmIA02/B02 at 4.0 cM/3.56 Mbp explained 9.06% of the phenotypic variance. The combined genotypic effects of both QTLs reduced smut incidence by 57% and were stable over the 3 years of evaluation. The genome regions containing the QTLs are rich in genes encoding proteins involved in plant defense, providing new insights into the genetic architecture of peanut smut resistance. CONCLUSIONS: A major QTL and a minor QTL identified in this study provide new insights into the genetic architecture of peanut smut resistance that may aid in breeding new varieties resistant to peanut smut.

Genotyping tools and resources to assess peanut germplasm: smut-resistant landraces as a case study.

Peanut smut caused by Thecaphora frezii is a severe fungal disease currently endemic to Argentina and Brazil. The identification of smut resistant germplasm is crucial in view of the potential risk of a global spread. In a recent study, we reported new sources of smut resistance and demonstrated its introgression into elite peanut cultivars. Here, we revisited one of these sources (line I0322) to verify its presence in the U.S. peanut germplasm collection and to identify single nucleotide polymorphisms (SNPs) potentially associated with resistance. Five accessions of Arachis hypogaea subsp. fastigiata from the U.S. peanut collection, along with the resistant source and derived inbred lines were genotyped with a 48K SNP peanut array. A recently developed SNP genotyping platform called RNase H2 enzyme-based amplification (rhAmp) was further applied to validate selected SNPs in a larger number of individuals per accession. More than 14,000 SNPs and nine rhAmp assays confirmed the presence of a germplasm in the U.S. peanut collection that is 98.6% identical (P < 0.01, bootstrap t-test) to the resistant line I0322. We report this germplasm with accompanying genetic information, genotyping data, and diagnostic SNP markers.

Introgression of peanut smut resistance from landraces to elite peanut cultivars (Arachis hypogaea L.).

Smut disease caused by the fungal pathogen Thecaphora frezii Carranza & Lindquist is threatening the peanut production in Argentina. Fungicides commonly used in the peanut crop have shown little or no effect controlling the disease, making it a priority to obtain peanut varieties resistant to smut. In this study, recombinant inbred lines (RILs) were developed from three crosses between three susceptible peanut elite cultivars (Arachis hypogaea L. subsp. hypogaea) and two resistant landraces (Arachis hypogaea L. subsp. fastigiata Waldron). Parents and RILs were evaluated under high inoculum pressure (12000 teliospores g-1 of soil) over three years. Disease resistance parameters showed a broad range of variation with incidence mean values ranging from 1.0 to 35.0% and disease severity index ranging from 0.01 to 0.30. Average heritability (h2) estimates of 0.61 to 0.73 indicated that resistance in the RILs was heritable, with several lines (4 to 7 from each cross) showing a high degree of resistance and stability over three years. Evidence of genetic transfer between genetically distinguishable germplasm (introgression in a broad sense) was further supported by simple-sequence repeats (SSRs) and Insertion/Deletion (InDel) marker genotyping. This is the first report of smut genetic resistance identified in peanut landraces and its introgression into elite peanut cultivars.

Mycorrhizal fungi symbiosis as a strategy against oxidative stress in soybean plants.

Oxidative stress responses generated by paraquat (PQ), an herbicide that triggers an oxidative stress reaction in leaves, were studied in non-arbuscular mycorrhizal (non-AM) and in arbuscular mycorrhizal (AM) soybean plants inoculated with Glomus mosseae (Gm) or Glomus intraradices (Gi). Some oxidative stress symptoms were evident in non-AM after 6 d of PQ application on leaves. Oxidative damage, measured as malondialdehyde content (MDA), was significantly higher, and although no changes were evident in total catalase (CAT, EC 1.11.1.6) and total superoxide dismutase (SOD, EC 1.15.1.1) activity, total ascorbate peroxidase (APX, EC 1.11.1.11) activity was significantly reduced. These effects were correlated with a significant decrease in growth parameters. By contrast, in both AM plants, foliar MDA content was reduced or unaltered and, interestingly, after PQ stress, its level was unchanged and significantly lower than in PQ non-AM plants. Unlike PQ stress in non-AM plants, total APX activity was unaltered or induced by AM plants, while total SOD activity was unchanged and no consistent effects were detected in total CAT activity. All these events coincided with no changes or a significant increase in growth parameters. Since oxidative stress is a common phenomenon triggered by several environmental stresses, these results highlight the importance of mycorrhizal fungi in oxidative stress regulation as a general strategy to protect plants from abiotic and biotic stress.