Stem rust, caused by Puccinia graminis f. sp. tritici (Pgt), threatens global wheat production. Development of cultivars with increased resistance to stem rust by identification, mapping, and deployment of resistance genes is the best strategy for controlling the disease. In this study, we performed fine mapping and characterization of the all-stage stem rust resistance (Sr) gene Sr8155B1 from the durum wheat line 8155-B1. In seedling tests of biparental populations, Sr8155B1 was effective against six Chinese Pgt races tested. In a segregating population of 5060 gametes, Sr8155B1 was mapped to a 0.06-cM region flanked by markers Pku2772 and Pku43365, corresponding to 1.5- and 2.7-Mb regions in the Svevo and Chinese Spring reference genomes. Both regions include several typical nucleotide-binding leucine-rich repeat (NLR) and protein kinase genes that represent candidate genes. Among them, three NLR genes and three receptor-like protein kinases were highly polymorphic between the parental lines and their transcripts were upregulated in the homozygous resistant line TdR2 relative to its susceptible sister line TdS4. Four markers (Pku2772, Pku43365, Pku2950, and Pku3721) developed in this study, together with seedling resistance responses, correctly predicted Sr8155B1 absence or presence in 78 tetraploid wheat genotypes tested. The presence of Sr8155B1 in tetraploid wheat accessions CItr 14916, PI 197492, and PI 197493 was confirmed by mapping in three F₂ populations. The genetic map and linked markers developed in this study may accelerate the deployment of Sr8155B1-mediated resistance in wheat breeding programs.

Leaf, spike, stem, and root morphologies are key factors that determine crop growth, development, and productivity. Multiple genes that control these morphological traits have been identified in Arabidopsis, rice, maize, and other plant species. However, little is known about the genomic regions and genes associated with morphological traits in wheat. Here, we identified the ethyl methanesulfonate-derived mutant wheat line M133 that displays multiple morphological changes that include upward-curled leaves, paired spikelets, dwarfism, and delayed heading. Using bulked segregant RNA sequencing (BSR-seq) and a high-resolution genetic map, we identified TraesCS1D02G155200 (HB-D2) as a potential candidate gene. HB-D2 encodes a class Ⅲ homeodomain-leucine zipper (HD-ZIP Ⅲ) transcription factor, and the mutation was located in the miRNA165/166 complementary site, resulting in a resistant allele designated rHb-D2. The relative expression of rHb2 in the mutant plants was significantly higher (P < 0.01) than in plants homozygous for the WT allele. Independent resistant mutations that disrupt the miRNA165/166 complementary sites in the A- (rHb-A2) and B-genome (rHb-B2) homoeologs showed similar phenotypic alterations, but the relative intensity of the effects was different. Transgenic plants expressing rHb-D2 gene driven by the maize UBIQUITIN (UBI) promoter showed similar phenotypes to the rHb-D2 mutant. These results confirmed that HB-D2 is the causal gene responsible for the mutant phenotypes. Finally, a survey of 1397 wheat accessions showed that the complementary sites for miRNA165/166 in all three HB2 homoeologs are highly conserved. Our results suggest that HB2 plays an important role in regulating growth and development in wheat.