Chromosome engineering-mediated introgression and molecular mapping of novel Aegilops speltoides-derived resistance genes for tan spot and Septoria nodorum blotch diseases in wheat.

Abstract

We identified, mapped and introduced novel Aegilops speltoides-derived resistance genes for tan spot and SNB diseases into wheat, enhancing understanding and utilization of host resistance to both diseases in wheat. Tan spot and Septoria nodorum blotch (SNB) are two important fungal diseases of wheat. Resistance to these diseases is often observed as the lack of sensitivity to the necrotrophic effectors (NE) produced by the fungal pathogens and thus exhibits a recessive inheritance pattern. In this study, we identified novel genes for resistance to tan spot and SNB on Aegilops speltoides (2n = 2x = 14, genome SS) chromosome 2S. These genes confer dominant resistance in the wheat background, indicating a distinct NE-independent mechanism of resistance. Ae. speltoides chromosome 2S was engineered for resistance gene introgression and molecular mapping by inducing meiotic homoeologous recombination with wheat chromosome 2B. Twenty representative 2B-2S recombinants were evaluated for reaction to tan spot and SNB and were delineated by genomic in situ hybridization and high-throughput wheat 90K SNP assay. The resistance genes physically mapped to the sub-telomeric region (~ 8Mb) on the short arm of chromosome 2S and designated TsrAes1 for tan spot resistance and SnbAes1 for SNB resistance. In addition, we developed SNP-derived PCR markers closely linked to TsrAes1/SnbAes1 for marker-assisted selection in wheat breeding. TsrAes1 and SnbAes1 are the first set of NE-independent tan spot, and SNB resistance genes are identified from Ae. speltoides. The 2SS-2BS·2BL recombinants with minimal amounts of Ae. speltoides chromatin containing TsrAes1/SnbAes1 were produced for germplasm development, making the wild species-derived resistance genes usable in wheat breeding. This will strengthen and diversify resistance of wheat to tan spot and SNB and facilitate understanding of resistance to these two diseases.