Yong Qiang Gu

Key message A total of 37 SNPs associated with resistance to five races of Pyrenophora tritici-repentis and two necrotrophic effectors were identified in a NAM population derived from synthetic and spring wheat. Abstract Tan spot, caused by Pyrenophora tritici-repentis, is a major foliar disease of wheat worldwide, and expanding the genetic basis of resistance remains a breeding priority. Synthetic hexaploid wheat (SHW) represents a valuable reservoir of novel alleles, yet its contribution to tan spot resistance has not been fully characterized. Here, a modified Nested Association Mapping population including 276 BC₁F₈ lines from crosses between four SHW parents and diverse hard red spring wheat (HRSW) cultivars was evaluated for reactions to five P. tritici-repentis races and two associated necrotrophic effectors (NEs) (Ptr ToxA and Ptr ToxB). The population exhibited broad phenotypic variation, with SHW parents and 66 BC₁F₈ lines showing resistance to all races. Genome-wide association analysis identified 21 marker-trait associations (MTAs) associated with tan spot resistance, of which, 6 resistance alleles were derived from SHW and 4 from HRSW parents, and 11 from both. Major-effect resistance loci were localized on chromosomes 5A, 2B, 5B, and 7D. Additionally, 14 MTAs were associated with Ptr ToxA sensitivity and 2 with Ptr ToxB sensitivity. Resistance alleles contributed by both parents showed a significant additive effect in reducing disease severity. Several loci colocalized with previously reported QTLs or genes, including Tsn1-B1 and Tsc2, while others represent potentially novel genomic regions. Notably, multiple lines were resistant to all races despite sensitivity to one or both NEs, indicating the presence of quantitative resistance other than those effector–sensitivity loci. These findings provide valuable genetic resources for facilitating marker‑assisted and genomic selection targeting tan spot resistance in wheat breeding.

Understanding plant resistance to insects has lagged owing to a scarcity of cloned resistance genes. Here we report cloning of the greenbug resistance gene Gb3 in wheat ( Triticum aestivum L.), initially introgressed into cultivars such as ‘TAM112’ from Aegilops tauschii . Gb3 encodes an intracellular kinase–pseudokinase protein, featuring a unique MAP3K-like domain. This gene probably originated through fusion, duplication and indel events in the Triticeae tribe, retaining its functionality in several Aegilops species. Transgenic Gb3 expression in the susceptible Fielder wheat enhanced resistance to multiple biotypes, while the Gb3 knockout in TAM112 resulted in susceptibility. Comprehensive analyses indicate that greenbugs preferentially feed on susceptible plants, inducing a prolonged oxidative stress response. Conversely, resistant plants expressing Gb3 mediate greenbug resistance by producing oxylipins and other defensive compounds. Our findings lay the groundwork for investigating plant–insect interactions and provide a crucial genetic resource for developing sustainable aphid resistance in cereal crops.

Fusarium head blight (FHB), caused by Fusarium graminearum, is one of the most devastating diseases of wheat (Triticum aestivum) and other cereal crops wor

Aegilops caudata L. is a rich source of resistance genes to major wheat pathogens and pests, yet its complex genome structure and lack of a reference sequence have hindered genetic analysis, gene discovery, and introgression. Here, we report a high-quality genome sequence assembly of Ae. caudata accession S740-69, integrated with optical mapping to precisely delineate introgressed segments from structurally altered genomic regions in wheat-Ae. caudata translocation lines carrying a novel stem rust resistance gene. Resequencing and phenotyping of 95 diverse accessions, coupled with k-mer-based association mapping, enabled population-level identification of several novel loci for resistance to wheat pests and diseases, such as greenbug and stem rust. Virus-induced gene silencing confirmed Aecau6C01G127270 (SrAect1) as the first functionally characterized stem rust resistance gene from Ae. caudata. This new genomic framework provides a foundation for systematic mining of resistance genes in this species and their efficient introgression into wheat.

Key message LMWgs Finder developed by this study was used to re-identify the LMW-GS genes in a total of 26 genomes across the grass family and several important and novel findings were obtained. Abstract LMW-GS are one of the primary components of wheat (Triticum aestivum L.) seed storage proteins, which have an important impact on wheat end-use quality traits. Identifying LMW-GS genes accurately within wheat genomes has consistently presented a significant challenge. LMWgsFinder developed by this study was used to re-identify the LMW-GS genes in a total of 26 genomes of the grass family. Apart from six species, a total of 291 LMW-GS genes were identified. Except for the two versions of the TaCS (Triticum aestivum Chinese Spring) genome, only 38.13% (98/257) of the LMW-GS genes identified by LMWgsFinder were annotated in the coding sequence annotation files (provided by the sequencing research groups) of the remaining 18 genomes. EnSpm-like transposon activity mediated recent duplication or triplication of the same LMW-GS gene has been observed in 8 wheat species for the first time, indicating that the replication of LMW-GS genes has been ongoing alongside the evolution of wheat. Several cases of rare structural variations associated with the loss or acquisition of LMW-GS gene function have been discovered and experimentally verified. Twenty-one new LMW-GS genes were discovered in 15 species of Triticeae. The results of this study provide the first empirical support at the DNA level, with confirmed chromosomal localization information, for the widely accepted notion that LMW-GS genes undergo gene duplication during wheat evolution. Additionally, this study offers gene sequence resources and a wealth of valuable information for further research on LMW-GS gene function, molecular-assisted selection, gene aggregation breeding, and molecular design breeding.

Fusarium head blight (FHB), mainly caused by Fusarium graminearum and Fusarium culmorum , is a major wheat disease. Significant efforts have been made to improve resistance to FHB in bread wheat ( Triticum aestivum ), but more work is needed for durum wheat ( Triticum turgidum spp. durum ). Bread wheat has ample genetic variation for resistance breeding, which can be readily exploited, while durum wheat is characterized by higher disease susceptibility and fewer valuable resistance sources. The Wheat Initiative – Expert Working Group on Durum Wheat Genomics and Breeding has promoted a scientific discussion to define the key actions that should be prioritized for achieving resistance in durum wheat comparable to that found in bread wheat. Here, a detailed state of the art and novel tools to improve FHB resistance in durum are presented, together with a perspective on the next steps forward. A meta‐analysis grouping all quantitative trait loci (QTL) associated with FHB resistance in both bread and durum wheat has been conducted to identify hotspot regions that do not overlap with Rht alleles, which are known to negatively correlate with FHB resistance. A detailed list of QTL related to FHB resistance and deoxynivalenol contamination and durum lines carrying different sources of FHB resistance are provided as a strategic resource. QTL, closely linked markers and durum wheat lines carrying the useful alleles, can be selected to design an effective breeding program. Finally, we highlight the priority actions that should be implemented to achieve satisfactory resistance to FHB in durum wheat.

Powdery mildew, caused by the fungal pathogen Blumeria graminis (DC.) E. O. Speer f. sp. tritici Em. Marchal ( Bgt ), is a constant threat to global wheat ( Triticum aestivum L.) production. Although ∼100 powdery mildew ( Pm ) resistance genes and alleles have been identified in wheat and its relatives, more is needed to minimize Bgt ’s fast evolving virulence. In tetraploid wheat ( Triticum turgidum L.), wild emmer wheat [ T. turgidum ssp. dicoccoides (Körn. ex Asch. & Graebn.) Thell.] accessions from Israel have contributed many Pm resistance genes. However, the diverse genetic reservoirs of cultivated emmer wheat [ T. turgidum ssp. dicoccum (Schrank ex Schübl.) Thell.] have not been fully exploited. In the present study, we evaluated a diverse panel of 174 cultivated emmer accessions for their reaction to Bgt isolate OKS(14)‐B‐3‐1 and found that 66% of accessions, particularly those of Ethiopian (30.5%) and Indian (6.3%) origins, exhibited high resistance. To determine the genetic basis of Bgt resistance in the panel, genome‐wide association studies were performed using 46,383 single nucleotide polymorphisms (SNPs) from genotype‐by‐sequencing and 4331 SNPs from the 9K SNP Infinium array. Twenty‐five significant SNP markers were identified to be associated with Bgt resistance, of which 21 SNPs are likely novel loci, whereas four possibly represent emmer derived Pm4a , Pm5a , PmG16 , and Pm64 . Most novel loci exhibited minor effects, whereas three novel loci on chromosome arms 2AS, 3BS, and 5AL had major effect on the phenotypic variance. This study demonstrates cultivated emmer as a rich source of powdery mildew resistance, and the resistant accessions and novel loci found herein can be utilized in wheat breeding programs to enhance Bgt resistance in wheat.

Antimicrobials have been important medicines used to treat various infections. However, some antibiotics increase the expression of Shiga toxin (Stx). Also, the pervasive use of persistent antibiotics has led to ecotoxicity and antibiotic resistance. In this study, a newly developed broad-spectrum and reversible antibiotic (guanylhydrazone disinfectant) was evaluated for its antibiotic activity and effects on Stx production and global transcription of bacteria. No Stx induction was observed in 25 Shiga toxin-producing E. coli (STEC) isolates treated with a sublethal concentration of the guanylhydrazone. A differential gene expression study comparing two guanylhydrazone-treated to non-treated E. coli strains indicated that the expression of a group of stress-responsive genes were enhanced. The Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that guanylhydrazone treatment significantly downregulated the pathways of ribosome and flagellar assembly in both pathogenic and non-pathogenic strains and differentially regulated some pathways essential for bacteria to maintain cell shape and gain survival advantage in two strains. In addition, upregulation of antibiotic resistant genes related to the multidrug efflux system and virulence genes coding for colibactin, colicin, and adhesin was observed in strains treated with the disinfectant. The knowledge obtained in this study contributes to our understanding of the mode of this disinfectant action and facilitates our effort to better use disinfectants for STEC treatments.