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Mitogen-activated protein kinases (MAPKs) have been demonstrated to be involved in fungal development, sexual reproduction, pathogenicity and/or virulence in many filamentous plant pathogenic fungi, but genes for MAPKs in the fungal cereal pathogen Bipolaris sorokiniana have not been characterized. In this study, orthologues of three MAPK genes (CsSLT2, CsHOG1 and CsFUS3) and one MAPK kinase kinase (MAPKKK) gene (CsSTE11) were identified in the whole genome sequence of the B. sorokiniana isolate ND90Pr, and knockout mutants were generated for each of them. The ∆Csfus3 and ∆Csste11 mutants were defective in conidiation and formation of appressoria-like structures, showed hypersensitivity to oxidative stress and lost pathogenicity on non-wounded leaves of barley cv. Bowman. When inoculated on wounded leaves of Bowman, the ∆Csfus3 and ∆Csste11 mutants were reduced in virulence compared to the wild type. No morphological changes were observed in the ∆Cshog1 mutants in comparison with the wild type; however, they were slightly reduced in growth under oxidative stress and were hypersensitive to hyperosmotic stress. The ∆Cshog1 mutants formed normal appressoria-like structures but were reduced in virulence when inoculated on Bowman leaves. The ∆Csslt2 mutants produced more vegetative hyphae, had lighter pigmentation, were more sensitive to cell wall degrading enzymes, and were reduced in virulence on Bowman leaves, although they formed normal appressoria like the wild type. Root infection assays indicated that the ∆Cshog1 and ∆Csslt2 mutants were able to infect barley roots while the ∆Csfus3 and ∆Csste11 failed to cause any symptoms. However, no significant difference in virulence was observed for ∆Cshog1 mutants while ∆Csslt2 mutants showed significantly reduced virulence on barley roots in comparison with the wild type. Our results indicated that all of these MAPK and MAPKKK genes are involved in the regulation of fungal development under normal and stress conditions and required for full virulence on barley plants.

Objective To develop a deep learning–based method with information fusion of US images and RF signals for better classification of thyroid nodules (TNs). Methods One hundred sixty-three pairs of US images and RF signals of TNs from a cohort of adult patients were used for analysis. We developed an information fusion–based joint convolutional neural network (IF-JCNN) for the differential diagnosis of malignant and benign TNs. The IF-JCNN contains two branched CNNs for deep feature extraction: one for US images and the other one for RF signals. The extracted features are fused at the backend of IF-JCNN for TN classification. Results Across 5-fold cross-validation, the accuracy, sensitivity, specificity, and area under the receiver operating characteristic curve (AUROC) obtained by using the IF-JCNN with both US images and RF signals as inputs for TN classification were respectively 0.896 (95% CI 0.838–0.938), 0.885 (95% CI 0.804–0.941), 0.910 (95% CI 0.815–0.966), and 0.956 (95% CI 0.926–0.987), which were better than those obtained by using only US images: 0.822 (0.755–0.878; p = 0.0044), 0.792 (0.679–0.868, p = 0.0091), 0.866 (0.760–0.937, p = 0.197), and 0.901 (0.855–0.948, p = .0398), or RF signals: 0.767 (0.694–0.829, p < 0.001), 0.781 (0.685–0.859, p = 0.0037), 0.746 (0.625–0.845, p < 0.001), 0.845 (0.786–0.903, p < 0.001). Conclusions The proposed IF-JCNN model filled the gap of just using US images in CNNs to characterize TNs, and it may serve as a promising tool for assisting the diagnosis of thyroid cancer. Key Points • Raw radiofrequency signals before ultrasound imaging of thyroid nodules provide useful information that is not carried by ultrasound images. • The information carried by raw radiofrequency signals and ultrasound images for thyroid nodules is complementary. • The performance of deep convolutional neural network for diagnosing thyroid nodules can be significantly improved by fusing US images and RF signals in the model as compared with just using US images.

Background Stem development is crucial for plant lodging, nutrients and water transport, and structural support for other organs. Understanding stem development and growth is essential for ensuring global food security. Although numerous lodging-resilient and high-yielding crop varieties have been developed in the Green Revolution by controlling plant height, the molecular mechanism underlying stem development, particularly for cereals, is not fully understood. The allelic stem mutants in barley ( Hordeum vulgare subsp. vulgare ),  single internode dwarf 1  ( sid1 ), provide a model system for genetic studies on stem development. Results We characterized and genetically analyzed the  sid1.b  mutation. To determine the precise position of  Sid1 , a high-resolution genetic map was constructed. Segregating F 2 plants derived from a cross between wild type (WT) and the mutant were genotyped with the barley 50 k iSelect SNP Array, and the detected SNPs were converted to PCR-based markers for fine mapping. The  Sid1  gene was mapped to a 429-kb region on chromosome 4H. Illumina sequencing of WT and sid1 identified a C → T transition in an epidermal pattern factor (EPF)-coding gene, which introduces a premature stop codon in the mutant allele. Conclusions In the present study, we genetically characterized and mapped the  sid1.a  mutation, which causes a dwarfed phenotype with single internode stems in barley. The EPF-encoding gene in the delimited region is a promising candidate for  Sid1 . Therefore, our study provides a foundation for cloning of  Sid1 , which will enhance our understanding of the molecular mechanisms underlying stem development, particularly in monocot plants.

Fusarium graminearum is the major causal agent of Fusarium head blight (FHB) in barley and wheat in North America. The fungus not only causes yield loss of the crops but also produces harmful trichothecene mycotoxins [Deoxynivalenol (DON) and its derivatives-3-acetyldeoxynivalenol (3ADON) and 15-acetyldeoxynivalenol (15ADON), and nivalenol (NIV)] that contaminate grains. Previous studies showed a dramatic increase of 3ADON-producing isolates with higher aggressiveness and DON production than the 15ADON-producing isolates in North America. However, the genetic and molecular basis of differences between the two types of isolates is unclear. In this study, we compared transcriptomes of the 3ADON and 15ADON isolates in vitro (in culture media) and in planta (during infection on the susceptible wheat cultivar 'Briggs') using RNA-sequencing. The in vitro gene expression comparison identified 479 up-regulated and 801 down-regulated genes in the 3ADON isolates; the up-regulated genes were mainly involved in C-compound and carbohydrate metabolism (18.6%), polysaccharide metabolism (7.7%) or were of unknown functions (57.6%). The in planta gene expression analysis revealed that 185, 89, and 62 genes were up-regulated in the 3ADON population at 48, 96, and 144 hours after inoculation (HAI), respectively. The up-regulated genes were significantly enriched in functions for cellular import, C-compound and carbohydrate metabolism, allantoin and allantoate transport at 48 HAI, for detoxification and virulence at 96 HAI, and for metabolism of acetic acid derivatives, detoxification, and cellular import at 144 HAI. Comparative analyses of in planta versus in vitro gene expression further revealed 2,159, 1,981 and 2,095 genes up-regulated in the 3ADON isolates, and 2,415, 2,059 and 1,777 genes up-regulated in the 15ADON isolates at the three time points after inoculation. Collectively, our data provides a foundation for further understanding of molecular mechanisms involved in aggressiveness and DON production of the two chemotype isolates of F. graminearum.

Key messageWe identified, fine mapped, and physically anchored a dominant spot blotch susceptibility gene Scs6 to a 125 kb genomic region containing the Mla locus on barley chromosome 1H.Spot blotch caused by Cochliobolus sativus is an important disease of barley, but the molecular mechanisms underlying resistance and susceptibility to the disease are not well understood. In this study, we identified and mapped a gene conferring susceptibility to spot blotch caused by the pathotype 2 isolate (ND90Pr) of C. sativus in barley cultivar Bowman. Genetic analysis of F1 and F2 progeny as well as F3 families from a cross between Bowman and ND 5883 indicated that a single dominant gene (designated as Scs6) conferred spot blotch susceptibility in Bowman. Using a doubled haploid (DH) population derived from a cross between Calicuchima-sib (resistant) and Bowman-BC (susceptible), we confirmed that Scs6, contributed by Bowman-BC, was localized at the same locus as the previously identified spot blotch resistance allele Rcs6, which was contributed by Calicuchima-sib and mapped on the short arm of chromosome 1H. Using a genome-wide putative linear gene index of barley (Genome Zipper), 13 cleaved amplified polymorphism markers were developed from 11 flcDNA and two EST sequences and mapped to the Scs6/Rcs6 region on a linkage map constructed with the DH population. Further fine mapping with markers developed from barley genome sequences and F2 recombinants derived from Bowman × ND 5883 and Bowman × ND B112 crosses delimited Scs6 in a 125 kb genomic interval harboring the Mla locus on the reference genome of barley cv. Morex. This study provides a foundational step for further cloning of Scs6 using a map-based approach.

Fusarium head blight (FHB) is a devastating disease in wheat. The use of resistant germplasm from diverse sources can significantly improve resistance to the disease. “Surpresa” is a Brazilian spring wheat cultivar with moderate FHB resistance, different from currently used sources. In this study, we aimed to identify and map the genetic loci for FHB resistance in Surpresa. A mapping population consisting of 187 recombinant inbred lines (RILs) was developed from a cross between Surpresa and a susceptible spring wheat cultivar, “Wheaton.” The population was evaluated for FHB by the point-inoculation method in three greenhouse experiments and four field trials between 2016 and 2018. Mean disease severity for Surpresa and Wheaton was 41.2 and 84.9% across the 3 years of experiments, ranging from 30.3 to 59.1% and 74.3 to 91.4%, respectively. The mean FHB severity of the NILs was 57%, with an overall range from 7 to 100%, suggesting transgressive segregation in the population. The population was genotyped using a two-enzyme genotyping-by-sequencing approach, and a genetic map was constructed with 5,431 single nucleotide polymorphism (SNP) markers. Four QTL for type II resistance were detected on chromosomes 3A, 5A, 6A, and 7A, explaining 10.4–14.4% of the total phenotypic variation. The largest effect QTL was mapped on chromosome 7A and explained 14.4% of the phenotypic variation; however, it co-localized with a QTL governing the days to anthesis trait. A QTL for mycotoxin accumulation was also detected on chromosome 1B, explaining 18.8% of the total phenotypic variation. The QTL for FHB resistance identified in the study may diversify the FHB resistance gene pool and increase overall resistance to the disease in wheat.

head blight (FHB) is one of the most destructive diseases in wheat worldwide. Breeding for FHB resistance is hampered by its complex genetic architecture, large genotype by environment interaction, and high cost of phenotype screening. Genomic selection (GS) is a powerful tool to enhance improvement of complex traits such as FHB resistance. The objectives of this study were to (1) investigate the genetic architecture of FHB resistance in a North Dakota State University (NDSU) hard red spring wheat breeding population, (2) test if the major QTL and play an important role in this breeding population; and (3) assess the potential of GS to enhance breeding efficiency of FHB resistance. A total of 439 elite spring wheat breeding lines from six breeding cycles were genotyped using genotyping-by-sequencing (GBS) and 102,147 SNP markers were obtained. Evaluation of FHB severity was conducted in 10 unbalanced field trials across multiple years and locations. One QTL for FHB resistance was identified and located on chromosome arm 1AL, explaining 5.3% of total phenotypic variation. The major type II resistance QTL only explained 3.1% of total phenotypic variation and the QTL was not significantly associated with FHB resistance in this breeding population. Our results suggest that integration of many genes with medium/minor effects in this breeding population should provide stable FHB resistance. Genomic prediction accuracies of 0.22-0.44 were obtained when predicting over breeding cycles in this study, indicating the potential of GS to enhance the improvement of FHB resistance.

Synthetic hexaploid wheat (SHW) can serve as a bridge for the transfer of useful genes from and tetraploid wheat ( ) into common wheat ( ). The objective of this study was to evaluate 149 SHW lines and their 74 tetraploid parents for their genetic diversity, breeding values and inter-genomic interactions for resistance to Fusarium head blight (FHB). The genetic diversity analysis was performed based on the population structure established using 4,674 and 3,330 polymorphic SNP markers among the SHW lines and tetraploid parents, respectively. The results showed that all and most accessions formed different clusters and subpopulations, respectively, whereas all the , , , and accessions were clustered together, suggesting that was more closely related to , , and than to . The genetic diversity of the SHW lines mainly reflected that of the tetraploid parents. The SHW lines and their tetraploid parents were evaluated for reactions to FHB in two greenhouse seasons and at two field nurseries for 2 years. As expected, most of the SHW lines were more resistant than their tetraploid parents in all environments. The FHB severities of the SHW lines varied greatly depending on the and tetraploid genotypes involved. Most of the SHW lines with a high level of FHB resistance were generally derived from the tetraploid accessions with a high level of FHB resistance. Among the 149 SHW lines, 140 were developed by using three accessions CIae 26, PI 268210, and RL 5286. These SHW lines showed FHB severities reduced by 21.7%, 17.3%, and 11.5%, respectively, with an average reduction of 18.3%, as compared to the tetraploid parents, suggesting that the D genome may play a major role in reducing disease severity in the SHW lines. Thirteen SHW lines consistently showed a high level of FHB resistance compared to the resistant check, Sumai 3, in each environment. These SHW lines will be useful for the development of FHB-resistant wheat germplasm and populations for discovery of novel FHB resistance genes.

Hexaploid‐derived resistance genes exhibit complex inheritance and expression patterns in tetraploid backgrounds. This study aimed to characterize the inheritance patterns and genomic compatibilities of hexaploid‐derived Fusarium head blight (FHB) resistance genes in tetraploid durum wheat (Triticum durum Desf.). Evaluation of FHB resistance for F1 hybrids of hexaploid ‘Sumai 3’ crossed with tetraploid and hexaploid wheats indicated that Sumai 3‐derived FHB resistance genes exhibit a dominant phenotypic effect seen only in hexaploid hybrids. Alternately, the hexaploid‐derived FHB resistance genes from PI 277012 exhibited complete dominance in the crosses with both tetraploid and hexaploid wheat. FHB evaluation of the F1 hybrids of Sumai 3 and PI 277012 crossed with ‘Langdon’ (LDN)–‘Chinese Spring’ D‐genome substitution lines suggested that chromosomes 2B, 3B, 4B, 5B, 6B, 3A, 4A, 6A, and 7A contain genes that suppress expression of the Sumai 3‐derived FHB resistance, whereas chromosomes 4A, 6A, and 6B contain genes required for expression of PI 277012‐derived FHB resistance. A wide range of segregation for FHB severity (10–90%) was observed in the F2 generation of Sumai 3 crossed with durum cultivars LDN and ‘Divide’, but the distribution of F3 families derived from the most resistant F2 segregants was skewed towards susceptibility. Similar segregation trends were observed in the crosses of PI 277012 with other durum wheats, whereby FHB resistance became slightly diluted over successive generations. These results suggest tetraploid durum wheat contains the unique alleles at multiple gene loci on different chromosomes that positively and/or negatively regulate the expression of hexaploid‐derived FHB resistance genes, which complicate efforts to deploy these genes in durum breeding programs. Core Ideas Durum contains genes that enhance or suppress hexaploid‐derived FHB resistance. The hexaploid‐derived FHB resistance genes were inherited differently in durum. Genomic compatibility for FHB resistance was assessed by D genome substitutions. Sumai 3‐derived FHB resistance was suppressed by loci on nine durum chromosomes. Three durum chromosomes contain loci needed for PI 277012‐derived FHB resistance.

Fusarium head blight (FHB), caused by Fusarium graminearum Schwabe, is one of the most devastating diseases in wheat (Triticum aestivum L.). The synthetic hexaploid wheat line Largo was developed from a cross between the durum wheat [T. turgidum ssp. durum (Desf.) Husn.] variety Langdon and the Aegilops tauschii Cosson accession PI 268210, and it was previously found to have a moderate level of FHB resistance. This study was conducted to identify quantitative trait loci (QTL) associated with FHB resistance using a population of 188 recombinant inbred lines (RILs) from a cross between Largo and the susceptible wheat line ND495. The RILs were evaluated for Type II resistance in two greenhouse and two field environments. The disease severity and 90K single‐nucleotide polymorphism marker data were used for QTL analysis, which revealed six QTL on chromosomes 1D, 2D, 5B, and 7D. Four QTL (QFhb.rwg‐1D, QFhb.rwg‐5B, QFhb.rwg‐7D.1, and QFhb.rwg‐7D.3) from Largo had minor effects, whereas two QTL (QFhb.rwg‐2D and QFhb.rwg‐7D.2) from ND495 showed large effects on FHB resistance. The result suggested that ND495 may possess suppressor or susceptibility gene(s) suppressing or masking FHB resistance controlled by the resistance QTL. Among these QTL, four coincided with previously reported QTL, including Fhb9, and two (QFhb.rwg‐1D and QFhb.rwg‐7D.1) are likely novel QTL. From the six QTL regions, 10 Kompetitive allele‐specific PCR markers were developed and validated for marker‐assisted selection. The QTL detected from the resistant and susceptible parents enhance our understanding of FHB resistance expression and provide new resources for improving FHB resistance in wheat. Core Ideas Synthetic wheat line Largo and spring wheat line ND495 are resistant and susceptible to Fusarium head blight (FHB), respectively. Quantitative trait loci (QTL) analysis for FHB resistance was performed using an ND495 × Largo population of 188 NIL lines. Six FHB‐resistant QTL were identified, with four and two from Largo and ND495, respectively. Two QTL from Largo are likely novel, whereas the other four coincided with previously reported QTL. Ten Kompetitive allele‐specific PCR markers for the six QTL were developed and validated. Plain Language Summary Fusarium head blight (FHB), commonly known as scab, is one of the most devastating diseases in wheat. A synthetic wheat line, Largo, developed from cross between durum wheat and goatgrass species Aegilops tauschii, was previously found to have FHB resistance. To identify the FHB resistance genes in Largo, we genetically analyzed a population of 188 pure lines developed from a cross between the susceptible wheat line ND495 and Largo with molecular markers and evaluated the population for FHB resistance in greenhouse and field nurseries. Based on genetic analysis, we identified six gene regions associated with FHB resistance, with two and four of the regions being derived from ND495 and Largo, respectively. The identified gene regions and their associated molecular markers provide new resources for wheat breeders in improving FHB resistance in modern wheat varieties.