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Cercospora leaf spot (CLS) is a major disease impacting global sugar beet cultivation and yield. This study investigated the potential diversity of Cercospora species causing CLS in Iranian sugar beet. Fungal isolates were characterized using integrated morphological and multi-gene sequence analyses. Subsequently, the possibility of rapid and specific diagnosis of the dominant pathogen using Loop-Mediated Isothermal Amplification (LAMP) was assessed. Infected leaves were collected from Ardabil, West Azerbaijan, Khorasan Razavi, Semnan, Mazandaran, Khuzestan, and Golestan provinces across the country. Genomic regions of actA , cmdA , gapdh , his3 and tef1 were amplified and sequenced. Phylogenetic results revealed that two species, Cercospora beticola and Cercospora gamsiana , are involved in causing cercospora leaf spot of sugar beet in Iran from which C. beticola was the dominant species. The LAMP-specific primers designed based on the gapdh gene region successfully discriminated C. beticola from C. gamsiana and other Cercospora species, as well as from some other fungal genera such as, Alternaria , Cladosporium, Curvularia, Ramularia and  Stemphylium. The LAMP assay in this study demonstrated a detection limit of 50 fg μL −1 . This study found C. beticola to be the dominant species in Iranian sugar beet fields. The LAMP technique proved effective for rapid, accurate diagnosis, aiding optimized disease management and control strategy selection.

Cercospora leaf spot, caused by the fungal pathogen Cercospora beticola, is the most destructive foliar disease of sugar beet worldwide. This review discusses C. beticola genetics, genomics, and biology and summarizes our current understanding of the molecular interactions that occur between C. beticola and its sugar beet host. We highlight the known virulence arsenal of C. beticola as well as its ability to overcome currently used disease management strategies. Finally, we discuss future prospects for the study and management of C. beticola infections in the context of newly employed molecular tools to uncover additional information regarding the biology of this pathogen. Taxonomy Cercospora beticola Sacc.; Kingdom Fungi, Phylum Ascomycota, Class Dothideomycetes, Order Capnodiales, Family Mycosphaerellaceae, Genus Cercospora. Host range Well‐known pathogen of sugar beet (Beta vulgaris subsp. vulgaris) and most species of the Beta genus. Reported as pathogenic on other members of the Chenopodiaceae (e.g., lamb's quarters, spinach) as well as members of the Acanthaceae (e.g., bear's breeches), Apiaceae (e.g., Apium), Asteraceae (e.g., chrysanthemum, lettuce, safflower), Brassicaceae (e.g., wild mustard), Malvaceae (e.g., Malva), Plumbaginaceae (e.g., Limonium), and Polygonaceae (e.g., broad‐leaved dock) families. Disease symptoms Leaves infected with C. beticola exhibit circular lesions that are coloured tan to grey in the centre and are often delimited by tan‐brown to reddish‐purple rings. As disease progresses, spots can coalesce to form larger necrotic areas, causing severely infected leaves to wither and die. At the centre of these spots are black spore‐bearing structures (pseudostromata). Older leaves often show symptoms first and younger leaves become infected as the disease progresses. Management Application of a mixture of fungicides with different modes of action is currently performed although elevated resistance has been documented in most employed fungicide classes. Breeding for high‐yielding cultivars with improved host resistance is an ongoing effort and prudent cultural practices, such as crop rotation, weed host management, and cultivation to reduce infested residue levels, are widely used to manage disease. Useful website https://www.ncbi.nlm.nih.gov/genome/11237?genome_assembly_id=352037 The hemibiotrophic fungus Cercospora beticola applies various virulence strategies to infect sugar beet and is currently only managed in‐field through integrated practices.

Frogeye leaf spot (FLS), caused by the fungus Cercospora sojina K. Hara, may cause a significant yield loss to soybean growers in regions with a warm and humid climate. Two soybean accessions, PI 594891 and PI 594774, were identified to carry a high level of resistance similar to that conditioned by the Rcs3 gene in 'Davis'. Previously, we reported that the resistance to FLS in these two plant introductions (PIs) was controlled by a novel gene (s) on chromosome 13 that is different from Rcs3. To fine-map the novel FLS resistance gene(s) in these two PIs, F2: 3 seeds from the crosses between PI 594891 and PI 594774, and the FLS susceptible genotype 'Blackhawk' were genotyped with SNP markers that were designed based on the SoySNP50k iSelect BeadChip data to identify recombinant events and locate candidate genes. Analysis of lines possessing key recombination events helped narrow down the FLS-resistance genomic region in PI 594891 from 3.3 Mb to a 72.6 kb region with five annotated genes. The resistance gene in PI 594774 was fine-mapped into a 540 kb region that encompasses the 72.6 kb region found in PI 594891. Sequencing five candidate genes in PI 594891 identified three genes that have several mutations in the promoter, intron, 5', and 3' UTR regions. qPCR analysis showed a difference in expression levels of these genes in both lines compared to Blackhawk in the presence of C. sojina. Based on phenotype, genotype and haplotype analysis results, these two soybean accessions might carry different resistance alleles of the same gene or two different gene(s). The identified SNPs were used to develop Kompetitive Allele Specific PCR (KASP) assays to detect the resistance alleles on chromosome 13 from the two PIs for marker-assisted selection.

Cercospora leaf spot (CLS), caused by Cercospora canescens , is a major threat to mungbean production worldwide. The disease is complicated by its wide host range, diverse pathogenic strains, and the influence of environmental factors. Understanding the interplay between the host, pathogen, and environmental conditions is crucial for developing effective control measures. In a bid to identify and validate CLS resistant mungbean genotypes we conducted multi-environment trials; Genomic selection of mungbean for resistance against CLS necessitates pre-identification in diverse environments. Initially, 110 genotypes were screened under controlled conditions in which thirty-day-old mungbean plants were thoroughly sprayed with the spore suspension using a glass atomizer. After three weeks of revalidation under controlled conditions, Koch’s postulates was adopted for disease identification before selecting 16 genotypes for field testing across four different environments over three successive years. The results obtained from the GGE biplot analysis emphasize the importance of taking both genetic and ambient factors in consideration when evaluating the potential of mungbean genotypes for resistance against CLS and therefore two genotypes “SK-89 (15)” and “WMB-9 (14)” was identified as desirable genotypes. The Additive Main Effects and Multiplicative Interaction (AMMI) model and the GGE biplot have emerged as potent tools for unraveling GEI complexities. It has expanded its application to include evaluation of resistant genotypes and to locate “ideal” evaluation sites and “mega environments” linked to resistance against infection. The study provides valuable insights for future breeding programs, allowing researchers to focus on incorporating these resistant traits into future varieties.

Sugar beet ( Beta vulgaris L. subsp. vulgaris ) is an important crop used not only in sugar production but also as the source of biogas and bioethanol, as a substrate in the petrochemical industry, and as a bio-resource for additional industrial and chemical feedstocks. Sugar beet is sensitive to environmental stress factors, including fungal infections such as Cercospora beticola (CLS—Cercospora leaf spot disease). Despite the introduction of plant cultivars with increased resistance to this disease, it causes a significant reduction in crop yield every year. The effect of infection is significant leaf loss in July and August, and the leaf rosette regeneration in September lasts until November. We examined three varieties of sugar beet with increased resistance to CLS. Using satellite images, we monitored the rate of leaf regeneration after CLS infection and studied in detail the gas exchange of plants, the efficiency of the photosynthetic apparatus, changes in the content of pigments and sugars in leaves, and sugar storage in roots. We showed for the first time that leaf regeneration after CLS infection seems independent of sugar accumulated in the roots. Sugar beetroot varieties were characterized by different strategies for managing sugar production and relocation. Moreover, the efficiency of CO 2 assimilation and solar energy absorption were not correlated in time and space in sugar beet, which, in the context of autumn leaf regeneration and senescence, may also be an indication for earlier harvesting.

Cercospora leaf blight (CLB) of soybean was believed to be caused only by Cercospora kikuchii worldwide. However, recent studies that include molecular phylogenetic analyses reveal that several cryptic species within Cercospora are associated with the disease. In a previous study, following a survey of commercial soybean fields in Santa Cruz, Bolivia, Cercospora spp. strains were isolated and identified as Cercospora cf. nicotianae based on morphological characteristics and by sequencing parts of the calmodulin, histone H3, and translation elongation factor 1-α genes and placing into a multilocus phylogeny. In the present study, pathogenicity tests were carried out in greenhouse assays on eleven soybean varieties which confirmed the infection and reproduction of the symptoms originally observed in the field. All the inoculated varieties were infected and showed CLB symptoms. Isolates were recovered from all soybean varieties tested and monoconidial cultures resembled original inoculum, completing Koch’s postulates. Thus, we confirm that according to the morphology of the conidia and cultures, pathogenicity tests, and molecular identification, C. cf. nicotianae is a causal agent of CLB of soybean.

Background Cercospora sojina is a fungal pathogen that causes frogeye leaf spot in soybean-producing regions, leading to severe yield losses worldwide. It exhibits variations in virulence due to race differentiation between strains. However, the candidate virulence-related genes are unknown because the infection process is slow, making it difficult to collect transcriptome samples. Results In this study, virulence-related differentially expressed genes (DEGs) were obtained from the highly virulent Race 15 strain and mildly virulent Race1 strain under nitrogen starvation stress, which mimics the physiology of the pathogen during infection. Weighted gene co-expression network analysis (WGCNA) was then used to find co-expressed gene modules and assess the relationship between gene networks and phenotypes. Upon comparison of the transcriptomic differences in virulence between the strains, a total of 378 and 124 DEGs were upregulated, while 294 and 220 were downregulated in Race 1 and Race 15, respectively. Annotation of these DEGs revealed that many were associated with virulence differences, including scytalone dehydratase, 1,3,8-trihydroxynaphthalene reductase, and β-1,3-glucanase. In addition, two modules highly correlated with the highly virulent strain Race 15 and 36 virulence-related DEGs were found to contain mostly β-1,4-glucanase, β-1,4-xylanas, and cellobiose dehydrogenase. Conclusions These important nitrogen starvation-responsive DEGs are frequently involved in the synthesis of melanin, polyphosphate storage in the vacuole, lignocellulose degradation, and cellulose degradation during fungal development and differentiation. Transcriptome analysis indicated unique gene expression patterns, providing further insight into pathogenesis.

Key message QTL-seq, linkage mapping, and whole-genome resequencing revealed a new locus ( qCLS5.1 ) controlling Cercospora canescens resistance in mungbean and Receptor-like protein 12 ( RLP12 ) genes as candidate genes for the resistance. Cercospora leaf spot (CLS) disease, caused by Cercospora canescens, is a common disease of mungbean ( Vigna radiata ). In this study, the genetics of CLS resistance was investigated in a new source of resistance (accession V2817) and the resistance was finely mapped to identify candidate genes. F 2 and F 2:3 populations of the cross V1197 (susceptible) × V2718 and a BC 1 F 1 population of the cross V1197 × (V1197 × V2817) were used in this study. Segregation analysis suggested that the resistance is controlled by a single dominant gene. QTL-seq using F 2 individuals revealed that a single QTL (designated qCLS5.1 ) on chromosome 5 controlled the resistance. The qCLS5.1 was confirmed in the F 2:3 and BC 1 F 1 populations by QTL analysis. Fine mapping using 978 F 2 individuals localized qCLS5.1 to a 48.94 Kb region containing three tandemly duplicated Receptor-like protein 12 ( RLP12 ) genes. Whole-genome resequencing and alignment of V1197 and V2817 revealed polymorphisms causing amino acid changes and premature stop codons in the three RLP12 genes. Collectively, these results show that qCLS5.1 is a new locus for CLS resistance in mungbean, and a cluster of RLP12 genes are candidate genes for the resistance. The new locus qCLS5.1 will be useful for molecular breeding of durable CLS-resistant mungbean cultivars.

Several mungbean ( Vigna radiata (L.) Wilczek) cultivars are susceptible to Cercospora leaf spot (CLS) caused by Cercospora canescens Ellis & Martin, and it is necessary to explore resistance sources and understand resistance mechanisms. However, the CLS resistance mechanisms have not yet been explored. The response to CLS revealed significantly different disease severity scores in both mungbean genotypes. Hypersensitive response (HR) started to appear at 2 days after inoculation (DAI) in SUPER5 but was never observed in CN84-1. SUPER5 exhibited fewer and smaller lesions than CN84-1 during CLS infection, resulting in SUPER5 being resistant while CN84-1 was susceptible to CLS. In this study, RNA sequencing (RNA-seq) analysis was used to unravel the mechanisms of resistance to CLS in a resistant line (SUPER5) and a susceptible variety (CN84-1) upon CLS infection. A total of 9510 DEGs including 4615 up-regulated and 4895 down-regulated genes were revealed. Of these 3242 and 1027 genes were uniquely up-regulated only in the SUPER5 and CN84-1, respectively, while 2902 and 734 genes were down-regulated only in SUPER5 and CN84-1, respectively. The 843 DEGs were enriched in biological processes mainly associated with plant defense responses, defense response to fungus, protein phosphorylation and response to chitin in Gene Ontology (GO) terms analysis. KEGG pathway analysis showed that these genes were represented in plant-pathogen interaction, the MAPK signaling pathway, plant hormone signal transduction, and cell wall component biosynthesis in response to the CLS infection specifically in SUPER5. In addition, the qRT-PCR was used to analyze the expression pattern of 22 candidate DEGs belonging to pathogenesis related (PR) proteins, resistance (R) proteins, transcription factors, hypersensitive response (HR), and the essential genes involved in cell wall activity during CLS-infected V. radiata . It was found that the expression of these genes was consistent with the RNA-seq analysis, showing a highly significant correlation with a coefficient of 0.7163 ( p  < 0.01). The co-expression network illustrated the interactions among these genes, which were involved in multiple functions related to the defense response. Interestingly, the ones encoding PR-2, thaumatin, peroxidase, defensin, RPM1, pectinesterase, chalcone synthase, auxin efflux carrier, and transcription factors (Pti1, Pti5, Pti6 and WRKY40) were highly significantly up-regulated in SUPER5 but not in CN84-1 upon CLS infection, suggesting that they might be involved in the CLS resistance mechanisms. Moreover, SUPER5 was found to have higher β-1,3-glucanase and chitinase activity levels than CN84-1. Our findings contribute to an understanding of the CLS resistance mechanisms and may advocate the development of more effective disease management approaches.

Key messageThis paper reports fine mapping of qCLS for resistance to Cercospora leaf spot disease in mungbean and identified LOC106765332encoding TATA-binding-protein-associated factor 5 (TAF5) as the candidate gene for the resistanceCercospora leaf spot (CLS) caused by the fungus Cercospora canescens is an important disease of mungbean. A QTL mapping using mungbean F2 and BC1F1 populations developed from the “V4718” (resistant) and “Kamphaeng Saen 1” (KPS1; susceptible) has identified a major QTL controlling CLS resistance (qCLS). In this study, we finely mapped the qCLS and identified candidate genes at this locus. A BC8F2 [KPS1 × (KPS1 × V4718)] population developed in this study and the F2 (KPS1 × V4718) population used in a previous study were genotyped with 16 newly developed SSR markers. QTL analysis in the BC8F2 and F2 populations consistently showed that the qCLS was mapped to a genomic region of ~ 13 Kb on chromosome 6, which contains only one annotated gene, LOC106765332 (designated “VrTAF5”), encoding TATA-binding-protein-associated factor 5 (TAF5), a subunit of transcription initiation factor IID and Spt-Ada-Gcn5 acetyltransferase complexes. Sequence comparison of VrTAF5 between KPS1 and V4718 revealed many single nucleotide polymorphisms (SNPs) and inserts/deletions (InDels) in which eight SNPs presented in eight different exons, and an SNP (G4,932C) residing in exon 8 causes amino acid change (S250T) in V4718. An InDel marker was developed to detect a 24-bp InDel polymorphism in VrTAF5 between KPS1 and V4718. Analysis by RT-qPCR showed that expression levels of VrTAF5 in KPS1 and V4718 were not statistically different. These results indicated that mutation in VrTAF5 causing an amino acid change in the VrTAF5 protein is responsible for CLS resistance in V4718.