Fungal disease meets its match: Fusarium head blight (FHB), caused by a fungus, reduces wheat crop yield and introduces toxins into the harvest. From the assembly of the genome of Thinopyrum elongatum , a wild relative of wheat used in breeding programs to improve cultivated wheat, Wang et al. cloned a gene that can address both problems (see the Perspective by Wulff and Jones). The encoded glutathione S -transferase detoxifies the trichothecene toxin and, when expressed in wheat, confers resistance to FHB. Science , this issue p. eaba5435 ; see also p. 822

Modern green revolution varieties of wheat (Triticum aestivum L.) confer semi-dwarf and lodging-resistant plant architecture owing to the Reduced height-B1b (Rht-B1b) and Rht-D1b alleles¹. However, both Rht-B1b and Rht-D1b are gain-of-function mutant alleles encoding gibberellin signalling repressors that stably repress plant growth and negatively affect nitrogen-use efficiency and grain filling^2–5. Therefore, the green revolution varieties of wheat harbouring Rht-B1b or Rht-D1b usually produce smaller grain and require higher nitrogen fertilizer inputs to maintain their grain yields. Here we describe a strategy to design semi-dwarf wheat varieties without the need for Rht-B1b or Rht-D1b alleles. We discovered that absence of Rht-B1 and ZnF-B (encoding a RING-type E3 ligase) through a natural deletion of a haploblock of about 500 kilobases shaped semi-dwarf plants with more compact plant architecture and substantially improved grain yield (up to 15.2%) in field trials. Further genetic analysis confirmed that the deletion of ZnF-B induced the semi-dwarf trait in the absence of the Rht-B1b and Rht-D1b alleles through attenuating brassinosteroid (BR) perception. ZnF acts as a BR signalling activator to facilitate proteasomal destruction of the BR signalling repressor BRI1 kinase inhibitor 1 (TaBKI1), and loss of ZnF stabilizes TaBKI1 to block BR signalling transduction. Our findings not only identified a pivotal BR signalling modulator but also provided a creative strategy to design high-yield semi-dwarf wheat varieties by manipulating the BR signal pathway to sustain wheat production.

Sprouting of grains in mature spikes before harvest is a major problem in wheat (Triticum aestivum) production worldwide. We cloned and characterized a gene underlying a wheat quantitative trait locus (QTL) on the short arm of chromosome 3A for preharvest sprouting (PHS) resistance in white wheat using comparative mapping and map-based cloning. This gene, designated TaPHS1, is a wheat homolog of a MOTHER OF FLOWERING TIME (TaMFT)-like gene. RNA interference-mediated knockdown of the gene confirmed that TaPHS1 positively regulates PHS resistance. We discovered two causal mutations in TaPHS1 that jointly altered PHS resistance in wheat. One GT-to-AT mutation generates a mis-splicing site, and the other A-to-T mutation creates a premature stop codon that results in a truncated nonfunctional transcript. Association analysis of a set of wheat cultivars validated the role of the two mutations on PHS resistance. The molecular characterization of TaPHS1 is significant for expediting breeding for PHS resistance to protect grain yield and quality in wheat production.

Fusarium head blight (FHB), caused primarily by Fusarium graminearum, has rapidly become the most devastating wheat disease worldwide. Host resistance is the most effective and sustainable strategy to combat the disease. To date, more than 50 unique quantitative trait loci (QTLs) have been identified in diverse wheat populations, and Fhb1 consistently shows the highest level of resistance in different genetic backgrounds. In spite of worldwide efforts to deploy Fhb1 through wheat breeding, only a few cultivars currently used in commercial production carry Fhb1. Recently, Fhb1 has been cloned and diagnostic markers have been developed, which will facilitate successful deployment of Fhb1 in wheat breeding. Using marker-assisted backcross, Fhb1 has been successfully transferred into locally adapted cultivars that carry minor QTLs, and selected Fhb1 lines in different backgrounds showed high levels of FHB resistance. This approach may provide a quick solution to improvement of FHB resistance in commercial cultivars. In addition, gene editing that knocks down the susceptible allele of Fhb1 in commercial cultivars may also improve wheat FHB resistance. Most other QTLs identified to date show much smaller effects than Fhb1. These QTLs are distributed in many locally adapted cultivars, and thus are important QTLs for FHB resistance improvement. Currently, diagnostic markers are still not available for most of these minor QTLs; therefore, genomic selection may improve selection accuracy for these QTLs to create highly FHB-resistant cultivars.