Peanut smut caused by Thecaphora frezii Carranza & Lindquist has been an issue for farmers and the peanut industry (Arachis hypogaea L.) in Argentina since the mid‐1990s. This disease causes pod malformation due to hypertrophy of seed tissues; in addition, colonized cells filled with teliospores give seeds a smutted mass appearance. Incidence may reach up to 52% in commercial plots, with up to 35% yield losses. Cultural management strategies and chemical treatment have not been effective; therefore, growing resistant varieties is likely to be the most effective control method for this disease. This study is aimed to identify sources of resistance in wild Arachis and to develop pre‐breeding materials for transferring the trait to cultivated peanut. After 3 yr of field trials using a randomized complete block design, the seven accessions of wild species assayed were resistant to smut. An amphidiploid [A. correntina (Burkart) Krapov. & W.C. Greg. × A. cardenasii Krapov. & W.C. Greg.] × A. batizocoi Krapov. & W.C. Greg.)4× was obtained and subsequently crossed with and experimental line of A. hypogaea for the development of a recombinant inbred line (RIL) population (89 lines). The RIL population showed a high phenotypic variability for resistance to peanut smut. The amphidiploid and 22 RILs were highly resistant, illustrating the effective transmission of resistance to peanut smut from the wild diploids into A. hypogaea. The development of RILs with resistance derived from wild species is a significant step towards the development of new peanut cultivars with different sources of resistance to peanut smut.

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.

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.

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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.

Sclerotinia minor causa el tizón del maní, enfermedad que ocasiona pérdidas en el cultivo. Este patógeno produce esclerocios como estructura de resistencia y se encuentra en forma agregada en el campo, lo que dificulta la evaluación de herramientas de control de la enfermedad. Es necesario el desarrollo de una técnica de inoculación que permita la homogeneidad de inóculo en cada unidad experimental. Los objetivos fueron: desarrollar y validar una metodología de inoculación a campo de S. minor en maní, y evaluar el comportamiento de diferentes genotipos del cultivo. Se aislaron y cuantificaron esclerocios de S. minor de muestras de suelo, se seleccionaron  Subpoblaciones y se produjo inóculo en dos medios de cultivo líquido. El inóculo generado se aplicó a campo sobre diez genotipos y se evaluó la intensidad de la enfermedad y la homogeneidad en la respuesta. El número de esclerocios en suelo fue de 0,81/100 gr antes y 2,07/100 gr después de la inoculación. S. minor creció en ambos medios de cultivo, pero el caldo papa presentó mayores ventajas. La técnica de inoculación fue exitosa, logrando que los valores de incidencia fueran homogéneos entre repeticiones. Se observaron diferencias estadísticamentesignificativas en el comportamiento de los genotipos frente a la enfermedad.

Sclerotinia blight is a soilborne disease caused by Sclerotinia minor Jagger and can produce severe decrease in yield. Cultural management strategies and chemical treatment are not completely effective; therefore, growing peanut‐resistant varieties is likely to be the most effective control method for this disease. Sclerotinia blight resistance has been identified in wild Arachis species and further transferred to peanut elite cultivars. To identify the genome regions conferring Sclerotinia blight resistance within a tetraploid genetic background, this study evaluated a population of recombinant inbred lines (RIL) with introgressed genes from three wild diploid species: A. cardenasii, A. correntina, and A. batizocoi. Two consistent quantitative trait loci (QTLs), qSbIA04 and qSbIB04 located on chromosomes A04 and B04, respectively, were identified. The QTL qSbIA04 was mapped at 56.39 cM explaining 29% of the phenotypic variance and qSbIB04 was mapped at 13.38 cM explaining 22% of the overall phenotypic variance.