Quantitative and Major-Gene Disease Resistance Loci in Wheat: A Structured Evidence Synthesis of Mapping, Validation and Cloning

Background. Wheat disease-resistance mapping identifies loci with different phenotypes and levels of biological evidence. Distinguishing quantitative disease resistance (QDR) from major-gene resistance, and marker validation from causal-gene identification, is necessary when prioritising loci for marker-assisted selection (MAS). Objectives. To synthesise evidence for mapped wheat disease-resistance loci, distinguish their resistance phenotypes and validation status, and assess the limits of cross-study positional comparisons. Methods. We assembled a structured evidence synthesis from author-curated literature, supplemented by searches of Semantic Scholar, PubMed, OpenAlex, and Scopus, and citation searching (English-language studies published in 2000–2025). The scope included mapped resistance loci in Triticum aestivum and T. durum, regardless of whether their phenotype was quantitative or major-gene resistance. We assessed resistance phenotype, developmental stage, tested pathogen spectrum, locus validation, and marker applicability separately. Genomic positions were retained in the source assembly; no coordinate realignment or statistical co-localisation analysis was performed. The evidence base is curated rather than exhaustive. Results. Forty-four studies covered 11 pathosystems, including Septoria tritici blotch caused by Zymoseptoria tritici. Nine focal loci illustrate differing evidence levels. Sbwm1, QYrcen.nwafu-7BL and QPm.caas-3BS have fine-mapping and marker-validation evidence; Fhb1 has causal-gene evidence from contextual studies outside the included set. Lr80, Stb19, Sb3 and Yr76 show major-gene phenotypes; Pm54 was also resolved as a Mendelian factor under the tested isolate. Independent validation is absent for Sb3 and Pm54. All 44 included studies were rated as having some concerns overall in the risk-of-bias assessment; structured extraction covers 39 of them. Conclusions. The synthesis supports prioritisation according to phenotype, causal evidence, and marker performance in the tested material. Reports of resistance loci on distal 3BS warrant further investigation, but the unresolved RefSeq position of Sb3 and the absence of harmonised interval tests prevent a claim of a verified cross-disease hotspot.