Inhibition of Aflatoxin Formation in Aspergillus Species by Peanut (Arachis hypogaea) Seed Stilbenoids in the Course of Peanut− Fungus Interaction

Common soil fungi, Aspergillus flavus and Aspergillus parasiticus, are opportunistic pathogens that invade preharvest peanut seeds. These fungi often produce carcinogenic aflatoxins that pose a threat to human and animal health through food chains and cause significant economic losses worldwide. Detection of aflatoxins and further processing of crops are mandated to ensure that contaminated agricultural products do not enter food channels. Under favorable conditions, the fungus-challenged peanut seeds produce phytoalexins, structurally related stilbenoids, capable of retarding fungal development. The purpose of the present study was to evaluate the potential influence of peanut phytoalexins on fungal development and aflatoxin formation in the course of peanut−fungus interaction. The present research revealed that during such interaction, aflatoxin formation was completely suppressed in A. flavus and A. parasiticus strains tested, when low concentrations of spores were introduced to wounded preincubated peanuts. In most of the experiments, when fungal spore concentrations were 2 orders of magnitude higher, the spores germinated and produced aflatoxins. Of all experimental seeds that showed fungal growth, 57.7% were aflatoxin-free after 72 h of incubation. The research provided new knowledge on the aflatoxin/phytoalexin formation in the course of peanut−fungus interaction

Suppression of Aflatoxin Production in \u3ci\u3eAspergillus\u3c/i\u3e Species by Selected Peanut (\u3ci\u3eArachis hypogaea\u3c/i\u3e) Stilbenoids

Aspergillus flavus is a soil fungus that commonly invades peanut seeds and often produces carcinogenic aflatoxins. Under favorable conditions, the fungus-challenged peanut plant produces and accumulates resveratrol and its prenylated derivatives in response to such an invasion. These prenylated stilbenoids are considered peanut antifungal phytoalexins. However, the mechanism of peanut−fungus interaction has not been sufficiently studied. We used pure peanut stilbenoids arachidin-1, arachidin-3, and chiricanine A to study their effects on the viability of and metabolite production by several important toxigenic Aspergillus species. Significant reduction or virtually complete suppression of aflatoxin production was revealed in feeding experiments in A. flavus, Aspergillus parasiticus, and Aspergillus nomius. Changes in morphology, spore germination, and growth rate were observed in A. flavus exposed to the selected peanut stilbenoids. Elucidation of the mechanism of aflatoxin suppression by peanut stilbenoids could provide strategies for preventing plant invasion by the fungi that produce aflatoxins

Evaluation of Leaf Spot Resistance in Wild \u3ci\u3eArachis\u3c/i\u3e Species of Section \u3ci\u3eArachis\u3c/i\u3e

Wild diploid Arachis species are potential sources of resistance to early (ELS) and late (LLS) leaf spot diseases caused by Passalora arachidicola (syn. Cercospora arachidicola Hori), and Nothopassalora personata (syn. Cercosporidium personatum (Berk. & Curt.) Deighton), respectively. Within section Arachis, limited information is available on the extent of genetic variation for resistance to these fungal pathogens. A collection of 78 accessions representing 15 wild species of Arachis section Arachis from the U.S peanut germplasm collection was evaluated for resistance to leaf spots. Screening was conducted under field (natural inoculum) conditions in Dawson, Georgia, during 2017 and 2018. Accessions differed significantly (P , 0.01) for all three disease variables evaluated, which included final defoliation rating, ELS lesion counts, and LLS lesion counts. Relatively high levels of resistance were identified for both diseases, with LLS being the predominant pathogen during the two years of evaluation. This research documents new sources of resistance to leaf spot diseases selected from an environment with high inoculum pressure. The presence of ELS and LLS enabled the selection of resistant germplasm for further introgression and pre-breeding

Transformation of Major Peanut (Arachis hypogaea) Stilbenoid Phytoalexins Caused by Selected Microorganisms

The peanut plant accumulates defensive stilbenoid phytoalexins in response to the presence of soil fungi, which in turn produce phytoalexin-detoxifying enzymes for successfully invading the plant host. Aspergillus spp. are opportunistic pathogens that invade peanut seeds; most common fungal species often produce highly carcinogenic aflatoxins. The purpose of the present research was to evaluate the in vitro dynamics of peanut phytoalexin transformation/detoxification by important fungal species. This work revealed that in feeding experiments, Aspergillus spp. from section Flavi were capable of degrading the major peanut phytoalexin, arachidin-3, into its hydroxylated homolog, arachidin-1, and a benzenoid, SB-1. However, Aspergillus niger from section Nigri as well as other fungal and bacterial species tested, which are not known to be involved in the infection of the peanut plant, were incapable of changing the structure of arachidin-3. The results of feeding experiments with arachidin-1 and resveratrol are also reported. The research provided new knowledge on the dynamics of peanut stilbenoid transformations by essential fungi. These findings may contribute to the elucidation of the phytoalexin detoxification mechanism involved in the infection of peanut by important toxigenic Aspergillus spp

Mitogenome and Nuclear-encoded Fungicide-target Genes of Thecaphora frezii - Causal Agent of Peanut Smut

Background: Thecaphora frezii Carranza and Lindquist causes smut disease in peanut (Arachis hypogaea L.) resulting in up to 35% yield losses. Fungicides have shown ineffective in controlling the disease; whereas research on the molecular basis of that fungicide resistance has been hindered because of the lack of genetic information about T. frezii. The goal of this work was to provide molecular information about fungicide-target loci in T. frezii, including its mitochondrial genome (mitogenome) and critical nuclear-encoded genes. Results: Here we report the complete annotated mitogenome of T. frezii, a 123,773 bp molecule containing the standard 14 genes that form part of mitochondrial complexes I, III, IV and V, 22 transfer RNAs, small and large subunits of ribosomal RNA, DNA polymerase, ribonuclease P, GII-reverse transcriptase/maturase, nine hypothetical open-reading frames and homing endonucleases (LAGLIDADG, GIY-YIG, HEG). In addition, we report the full-length cDNA sequence of T. frezii cytochrome b (cob) and cytochrome oxidase 1 (cox1) genes; as well as partial sequences of T. frezii succinate dehydrogenase (sdhb), ergosterol biosynthesis (Erg4), cytochrome P450 (cyp51), and beta tubulin (β-tubulin) genes, which are respective targets of strobilurins, quinone oxidation inhibitors, triazoles and beta-tubulin inhibitor fungicides commonly used in the peanut crop. Translation of cob and sdhb genes in this particular T. frezii isolate suggests potential resistance to strobilurin and carboxamide fungicides. Conclusion: The mitogenome and nuclear-encoded gene sequences presented here provide the molecular tools to research T. frezii fungicide-target loci

First draft genome and transcriptome of \u3ci\u3eCercosporidium personatum\u3c/i\u3e, causal agent of late leaf spot disease of peanut

Objective Two main fungal leaf spot diseases occur in peanut, namely early leaf spot (ELS) and late leaf spot (LLS), these cause a yearly average of $44 million losses. Limited genetic information, 3534 bp of sequencing, exists about the causal agent of LLS, Cercosporidium personatum (syn. Nothopassalora personata, syn. Phaeoisariopsis personata). The extremely slow growth of this fungus, approximately 1 cm colony in 6 months, and challenges in nucleic acid extractions have hindered research on LLS. Our goal in this work is to provide a reference genome for research on this pathogen. Results Whole genome and transcriptome sequencing of the LLS fungus were obtained. A total of 233,542,110 reads of the genome were de novo assembled resulting in 1061 scaffolds, and estimated genome size 27,597,787 bp. RNA sequencing resulted in 11,848,198 reads that were de novo assembled into 13,343 contigs. Genome annotation resulted in 10,703 putative genes. BUSCO analysis of the genome and annotation resulted in 91.1% and 89.5% completeness, respectively. Phylogenetic dendrograms for 5442 bp and 4401 bp of RNA Polymerase II largest and second largest subunits, and for 5474 bp of the ribosomal RNA cistron of C. personatum are presented in relation to closely related fungi

First draft genome of \u3ci\u3eThecaphora frezii\u3c/i\u3e, causal agent of peanut smut disease

Objectives: The fungal pathogen Thecaphora frezii Carranza & Lindquist causes peanut smut, a severe disease currently endemic in Argentina. To study the ecology of T. frezii and to understand the mechanisms of smut resistance in peanut plants, it is crucial to know the genetics of this pathogen. The objective of this work was to isolate the pathogen and generate the first draft genome of T. frezii that will be the basis for analyzing its potential genetic diversity and its interaction with peanut cultivars. Our research group is working to identify peanut germplasm with smut resistance and to understand the genetics of the pathogen. Knowing the genome of T. frezii will help analyze potential variants of this pathogen and contribute to develop enhanced peanut germplasm with broader and long-lasting resistance. Data description: Thecaphora frezii isolate IPAVE 0401 (here referred as T.f.B7) was obtained from a single hyphal-tip culture, its DNA was sequenced using Pacific Biosciences Sequel II (PacBio) and Illumina NovaSeq6000 (Nova). Data from both sequencing platforms were combined and the de novo assembling estimated a 29.3 Mb genome size. Completeness of the genome examined using Benchmarking Universal Single-Copy Orthologs (BUSCO) showed the assembly had 84.6% of the 758 genes in fungi_odb10

First draft genome of Thecaphora frezii, causal agent of peanut smut disease

Objectives: The fungal pathogen Thecaphora frezii Carranza & Lindquist causes peanut smut, a severe disease currently endemic in Argentina. To study the ecology of T. frezii and to understand the mechanisms of smut resistance in peanut plants, it is crucial to know the genetics of this pathogen. The objective of this work was to isolate the pathogen and generate the first draft genome of T. frezii that will be the basis for analyzing its potential genetic diversity and its interaction with peanut cultivars. Our research group is working to identify peanut germplasm with smut resistance and to understand the genetics of the pathogen. Knowing the genome of T. frezii will help analyze potential variants of this pathogen and contribute to develop enhanced peanut germplasm with broader and long-lasting resistance. Data description: Thecaphora frezii isolate IPAVE 0401 (here referred as T.f.B7) was obtained from a single hyphal-tip culture, its DNA was sequenced using Pacific Biosciences Sequel II (PacBio) and Illumina NovaSeq6000 (Nova). Data from both sequencing platforms were combined and the de novo assembling estimated a 29.3 Mb genome size. Completeness of the genome examined using Benchmarking Universal Single-Copy Orthologs (BUSCO) showed the assembly had 84.6% of the 758 genes in fungi_odb10.Instituto de Patología VegetalFil: Arias, Renee S. USDA-ARS National Peanut Research Laboratory (NPRL); Estados UnidosFil: Conforto, Erica Cinthia. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patología Vegetal; ArgentinaFil: Conforto, Erica Cinthia. Consejo Nacional de Investigaciones Científicas y Técnicas. Unidad de Fitopatología y Modelización Agrícola (UFyMA); ArgentinaFil: Orner, Valerie A. USDA-ARS National Peanut Research Laboratory (NPRL); Estados UnidosFil: Carloni, Edgardo José. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Fisiología y Recursos Genéticos Vegetales; ArgentinaFil: Soave, Juan H. El Carmen S.A.; ArgentinaFil: Massa, Alicia N. USDA-ARS National Peanut Research Laboratory (NPRL); Estados UnidosFil: Lamb, Marshall C. USDA-ARS National Peanut Research Laboratory (NPRL); Estados UnidosFil: Bernanrdi Lima, Nelson. Consejo Nacional de Investigaciones Científicas y Técnicas. Unidad de Fitopatología y Modelización Agrícola (UFyMA); ArgentinaFil: Bernanrdi Lima, Nelson. Instituto Nacional de Tecnología Agropecuaria (INTA). Instituto de Patología Vegetal; ArgentinaFil: Rago, Alejandro Mario. Instituto Nacional de Tecnología Agropecuaria (INTA). Centro de Investigaciones Agropecuarias (CIAP); ArgentinaFil: Rago, Alejandro Mario. Consejo Nacional de Investigaciones Científicas y Técnicas. Unidad de Fitopatología y Modelización Agrícola (UFyMA); Argentin

Two QTLs govern the resistance to Sclerotinia minor in an interspecific peanut RIL population

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