Bread wheat is one of the most important and broadly studied crops. However, due to the complexity of its genome and incomplete genome collection of wild populations, the bread wheat genome landscape and domestication history remain elusive. By investigating the whole-genome resequencing data of 93 accessions from worldwide populations of bread wheat and its diploid and tetraploid progenitors, together with 90 published exome-capture data, we find that the B subgenome has more variations than A and D subgenomes, including SNPs and deletions. Population genetics analyses support a monophyletic origin of domesticated wheat from wild emmer in northern Levant, with substantial introgressed genomic fragments from southern Levant. Southern Levant contributes more than 676 Mb in AB subgenomes and enriched in the pericentromeric regions. The AB subgenome introgression happens at the early stage of wheat speciation and partially contributes to their greater genetic diversity. Furthermore, we detect massive alien introgressions that originated from distant species through natural and artificial hybridizations, resulting in the reintroduction of ~ 709 Mb and ~ 1577 Mb sequences into bread wheat landraces and varieties, respectively. A large fraction of these intra- and inter-introgression fragments are associated with quantitative trait loci of important traits, and selection events are also identified. We reveal the significance of multiple introgressions from distant wild populations and alien species in shaping the genetic components of bread wheat, and provide important resources and new perspectives for future wheat breeding.

In contrast to large‐effect qualitative disease resistance, quantitative disease resistance (QDR) exhibits partial and generally durable resistance and has been extensively utilized in crop breeding. The molecular mechanisms underlying QDR remain largely unknown but considerable progress has been made in this area in recent years. In this review, we summarize the genes that have been associated with plant QDR and their biological functions. Many QDR genes belong to the canonical resistance gene categories with predicted functions in pathogen perception, signal transduction, phytohormone homeostasis, metabolite transport and biosynthesis, and epigenetic regulation. However, other “atypical” QDR genes are predicted to be involved in processes that are not commonly associated with disease resistance, such as vesicle trafficking, molecular chaperones, and others. This diversity of function for QDR genes contrasts with qualitative resistance, which is often based on the actions of nucleotide‐binding leucine‐rich repeat (NLR) resistance proteins. An understanding of the diversity of QDR mechanisms and of which mechanisms are effective against which classes of pathogens will enable the more effective deployment of QDR to produce more durably resistant, resilient crops.

Summary: Southern leaf blight (SLB), caused by the necrotrophic fungal pathogen Cochliobolus heterostrophus (anamorph Bipolaris maydis), is a major foliar disease which causes significant yield losses in maize worldwide. A major quantitative trait locus, qSLB_3.04, conferring recessive resistance to SLB was previously mapped on maize chromosome 3. Using a combination of map‐based cloning, association analysis, ethyl methanesulfonate and transposon mutagenesis, and CRISPR‐Cas9 editing, we demonstrate that a leucine‐rich repeat receptor‐like kinase gene which we have called ChSK1 (Cochliobolus heterostrophus Susceptibility Kinase 1) at qSLB_3.04 causes increased susceptibility to SLB. Genes of this type have generally been associated with the defense response. We present evidence that ChSK1 may be associated with suppression of the basal immune response. These findings contribute to our understanding of plant disease susceptibility genes and the potential to use them for engineering durable disease resistance.

Maize production is constantly threatened by the presence of different fungal pathogens worldwide. Genetic resistance is the most favorable approach to reducing yield losses resulted from fungal diseases. The molecular mechanism underlying disease resistance in maize remains largely unknown. The objective of this study was to identify key genes/pathways that are consistently associated with multiple fungal pathogen infections in maize. Here, we conducted a meta-analysis of gene expression profiles from seven publicly available RNA-seq datasets of different fungal pathogen infections in maize. We identified 267 common differentially expressed genes (co-DEGs) in the four maize leaf infection experiments and 115 co-DEGs in all the seven experiments. Functional enrichment analysis showed that the co-DEGs were mainly involved in the biosynthesis of diterpenoid and phenylpropanoid. Further investigation revealed a set of genes associated with terpenoid phytoalexin and lignin biosynthesis, as well as potential pattern recognition receptors and nutrient transporter genes, which were consistently up-regulated after inoculation with different pathogens. In addition, we constructed a weighted gene co-expression network and identified several hub genes encoding transcription factors and protein kinases. Our results provide valuable insights into the pathways and genes influenced by different fungal pathogens, which might facilitate mining multiple disease resistance genes in maize.