Abstract
Stripe or yellow rust (YR), caused by Puccinia striiformis Westend. f. sp. tritici (Pst), is a devastating fungal disease of wheat. Here, we report the map-based cloning of Yr26 (synonyms: Yr24, YrCH42, and YrG22), a major stripe rust resistance gene, and its validation by gene silencing, mutation analysis and transgenic complementation. Yr26, which firstly arises in emmer wheat and recently has introgressed into bread wheat, is a newly evolved gene encoding a transmembrane protein. AlphaFold v3.0 predictes a C-terminal four-helical bundle domain that is critical for triggering Ca2+-dependent cell death, a hallmark of the hypersensitive response. The cloning of Yr26 offers not only a genetic resource for pyramiding stripe rust resistance genes in wheat breeding but also an opportunity to study host–pathogen co-evolution.
Acknowledgements
The authors thank all members of the plant immunity research team in the State Key Laboratory of Crop Stress Resistance and High-Efficiency Production at Northwest A&F University for helpful comments. We are grateful to Prof. R.A. McIntosh, Plant Breeding Institute, University of Sydney, for language editing and proofreading of the draft manuscript; Drs. Jian Ma, Jun Li, Hongqing Ling, Xiaojun Nie, Meng Wang and Lin Huang for providing tetraploid wheat accessions; Drs. Zhiyong Liu, Jian Chen, and Yajun Wang for helpful suggestions and discussion; Drs. Xueling Huang for assistance with genetic transformation and KASP genotyping; Hua Zhao for assistance with confocal microscopy; Ms Haiying Wang for construction of a genomic DNA library; and Dr. Guohao Han for assistance with the provision of the pCAMBIA1305-GFP vector.
Funding
Research work conducted in China was supported by the National Natural Science Foundation of China (Grant No. 32293240, 32372562, 32302377, 32272088), Key R&D Program of Shaanxi (2024NC2-GJHX-36), and China Agriculture Research System (CARS-3). Research work on Yr24 cloning was supported by the Australian Research Council (Project DE170100151).
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Liu, S., Mu, K., Yang, S. et al. A transmembrane protein confers the Yr26/Yr24/YrCH42/YrG22-mediated stripe rust resistance in wheat. Nat Commun (2026). https://doi.org/10.1038/s41467-026-76091-5
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DOI: https://doi.org/10.1038/s41467-026-76091-5
Facts Only
* Yr26 (also known as Yr24, YrCH42, and YrG22) is a stripe rust resistance gene in wheat.
* The gene encodes a transmembrane protein.
* The gene originated in emmer wheat and was introgressed into bread wheat.
* Validation methods included gene silencing, mutation analysis, and transgenic complementation.
* AlphaFold v3.0 predicts a C-terminal four-helical bundle domain in the protein.
* This domain triggers Ca2+-dependent cell death.
* The disease is caused by the fungus Puccinia striiformis Westend. f. sp. tritici.
* Research was supported by the National Natural Science Foundation of China, Key R&D Program of Shaanxi, China Agriculture Research System, and the Australian Research Council.
* Institutional contributors include Northwest A&F University and the Plant Breeding Institute at the University of Sydney.
* The findings were published in Nature Communications (2026).
Executive Summary
Researchers have successfully cloned Yr26, a major resistance gene that protects wheat from stripe rust (yellow rust), caused by the fungus Puccinia striiformis Westend. f. sp. tritici. This gene, which originated in emmer wheat and was subsequently introgressed into bread wheat, encodes a transmembrane protein. Validation was achieved through a combination of gene silencing, mutation analysis, and transgenic complementation.
AlphaFold v3.0 predictions indicate that a C-terminal four-helical bundle domain within the protein is essential for triggering Ca2+-dependent cell death, a primary mechanism of the hypersensitive response used by plants to halt pathogen spread. This discovery provides a specific genetic resource for breeding programs aiming to pyramid multiple resistance genes to ensure more durable crop protection and offers a new model for studying the co-evolution of hosts and pathogens.
Full Take
This study utilizes ACADEMIC MODE. The methodology appears robust, employing a "gold standard" triad of validation: silencing (loss of function), mutation analysis (genetic confirmation), and complementation (gain of function). However, a peer reviewer would likely scrutinize the reliance on AlphaFold v3.0 for the functional assignment of the C-terminal domain. While predictive modeling is powerful, the transition from a predicted structure to a definitive claim about Ca2+-dependent cell death requires empirical biochemical evidence—such as calcium imaging or specific mutant assays—to move beyond correlation.
The claims regarding the "newly evolved" nature of the gene are proportionate to the discovery of its origin in emmer wheat, though the specific evolutionary timeline remains an area for further investigation. This work extends the existing knowledge of the wheat "resistome" by identifying a transmembrane protein mechanism, shifting the focus toward the physical architecture of the cell membrane in pathogen recognition.
In a real-world agricultural context, the utility of Yr26 depends on the current virulence profiles of Pst races in the field. If the pathogen has already evolved to evade Yr26, the gene's value is limited to "pyramiding"—combining it with other genes to increase the evolutionary cost for the fungus to break resistance.
To strengthen these findings, future research should focus on identifying the specific fungal effector that Yr26 recognizes. Does this protein act as a direct receptor or an indirect signaling component?
Bridge Questions:
1. How does the efficacy of Yr26 vary across different wheat cultivars?
2. Can the four-helical bundle domain be engineered into other cereal crops to confer similar resistance?
Sentinel — Human
This text exhibits the formal, dense, and methodologically focused language characteristic of a peer-reviewed scientific publication, indicating a high degree of human authorship within the specialized field.