Heading date (HD) in wheat determines geographic adaptation, seasonal performance, and ultimately affects yield and quality. However, the genetic regulation of HD remains unclear. Here, we identified an Ethyl Methane Sulfonate (EMS)-induced wheat mutant, je0072, which headed two days earlier than the wild-type (WT) cultivar Jing411 without significant changes in yield components. Bulked segregant analysis (BSA) using an F₂ population of 618 individuals identified the early-heading locus to the long arm of chromosome 5D. Genetic fine mapping further narrowed the locus to a 460-kb interval containing 10 high-confidence genes based on the Chinese Spring v2.1 reference genome. Sequence variation analysis identified a candidate gene, TaBGLU1-5D, encoding β-glycosyl hydrolase 1, which harbored a T-to-C substitution at position 31. Functional validation using independent mutants confirmed the role of TaBGLU1-5D in regulating HD. Transcriptome sequencing revealed that differentially expressed genes (DEGs) between WT and je0072 spikes at the heading stage were significantly enriched in starch and sucrose metabolism pathways. Weighted Gene Co-expression Network Analysis (WGCNA) further identified MADS-box transcription factor TaMADS26 as a regulatory hub associated with TaBGLU1-5D. We also found that TaBGLU1-5D modulates expression of key heading date-related genes, including VRN1, VRN3, and VRT2, thereby influencing HD. These results provide new insights into the genetic control of HD in wheat, and offer valuable resources for HD optimization in breeding programs.

Flag leaf angle is one of the key target traits in high yield wheat breeding. A smaller flag leaf angle reduces shading and enables plants to grow at a higher density, which increases yield. Here we identified a mutant, je0407, with an 84.34%–89.35% smaller flag leaf angle compared with the wild type. The mutant also had an abnormal lamina joint and no ligule or auricle. Genetic analysis indicated that the ligule was controlled by two recessive genes, which were mapped to chromosomes 2AS and 2DL. The mutant allele on chromosome 2AS was named Tafla1b, and it was fine mapped to a 1 Mb physical interval. The mutant allele on chr. 2DL was identified as Taspl8b, a novel allele of TaSPL8 with a missense mutation in the second exon, which was used to develop a cleaved amplified polymorphic sequence marker. F₃ and F₄ lines derived from crosses between Jing411 and je0407 were genotyped to investigate interactions between the Tafla1b and Taspl8b alleles. Plants with the Tafla1b/Taspl8a genotype had 58.41%–82.76% smaller flag leaf angles, 6.4%–24.9% shorter spikes, and a greater spikelet density (0.382 more spikelets per cm) compared with the wild type. Plants with the Tafla1a/Taspl8b genotype had 52.62%–82.24% smaller flag leaf angles and no differences in plant height or spikelet density compared with the wild type. Tafla1b/Taspl8b plants produced erect leaves with an abnormal lamina joint. The two alleles had dosage effects on ligule formation and flag leaf angle, but no significant effect on thousand-grain weight. The mutant alleles provide novel resources for improvement of wheat plant architecture.

Lesion mimic often exhibits leaf disease-like symptoms even in the absence of pathogen infection, and is characterized by a hypersensitive-response (HR) that closely linked to plant disease resistance. Despite this, only a few lesion mimic genes have been identified in wheat. In this investigation, a lesion mimic wheat mutant named je0297 was discovered, showing no alteration in yield components when compared to the wild type (WT). Segregation ratio analysis of the F₂ individuals resulting from the cross between the WT and the mutant revealed that the lesion mimic was governed by a single recessive gene in je0297. Using Bulked segregant analysis (BSA) and exome capture sequencing, we mapped the lesion mimic gene designated as lm6 to chromosome 6BL. Further gene fine mapping using 3315 F₂ individuals delimited the lm6 within a 1.18 Mb region. Within this region, we identified 16 high-confidence genes, with only two displaying mutations in je0297. Notably, one of the two genes, responsible for encoding flavonol synthase, exhibited altered expression levels. Subsequent phenotype analysis of TILLING mutants confirmed that the gene encoding flavonol synthase was indeed the causal gene for lm6. Transcriptome sequencing analysis revealed that the DEGs between the WT and mutant were significantly enriched in KEGG pathways related to flavonoid biosynthesis, including flavone and flavonol biosynthesis, isoflavonoid biosynthesis, and flavonoid biosynthesis pathways. Furthermore, more than 30 pathogen infection-related (PR) genes exhibited upregulation in the mutant. Corresponding to this expression pattern, the flavonoid content in je0297 showed a significant decrease in the 4^th leaf, accompanied by a notable accumulation of reactive oxygen, which likely contributed to the development of lesion mimic in the mutant. This investigation enhances our comprehension of cell death signaling pathways and provides a valuable gene resource for the breeding of disease-resistant wheat.