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Genomics accelerated isolation of a new stem rust avirulence gene–wheat resistance gene pair
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Edité par CCSD ; Nature Publishing Group -
International audience. Stem rust caused by the fungus Puccinia graminis f. sp. tritici (Pgt) is a devastating disease of the global staple crop wheat. Although this disease was largely controlled in the latter half of the twentieth century, new virulent strains of Pgt, such as Ug99, have recently evolved 1,2. These strains have caused notable losses worldwide and their continued spread threatens global wheat production. Breeding for disease resistance provides the most cost-effective control of wheat rust diseases 3. A number of rust resistance genes have been characterized in wheat and most encode immune receptors of the nucleotide-binding leucine-rich repeat (NLR) class 4 , which recognize pathogen effector proteins known as avirulence (Avr) proteins 5. However, only two Avr genes have been identified in Pgt so far, AvrSr35 and AvrSr50 (refs. 6,7), and none in other cereal rusts 8,9. The Sr27 resistance gene was first identified in a wheat line carrying an introgression of the 3R chromosome from Imperial rye 10. Although not deployed widely in wheat, Sr27 is widespread in the artificial crop species Triticosecale (triticale), which is a wheat-rye hybrid and is a host for Pgt 11,12. Sr27 is effective against Ug99 (ref. 13) and other recent Pgt strains 14,15. Here, we identify both the Sr27 gene in wheat and the corresponding AvrSr27 gene in Pgt and show that virulence to Sr27 can arise experimentally and in the field through deletion mutations, copy number variation and expression level polymorphisms at the AvrSr27 locus. The wheat stem rust isolate Pgt21-0 is avirulent on Sr27, but derivatives of this strain with virulence to Sr27 have been detected in the field 16,17 , suggesting that it may be heterozygous for AvrSr27. We therefore selected for spontaneous virulent rust mutants after inoculation of Pgt21-0 onto the resistant triticale cultivar 'Coorong' carrying Sr27. Three large single pustules were selected, purified in isolation and re-inoculated onto Coorong to confirm their virulent phenotype (Fig. 1a and Supplementary Fig. 1). We generated Illumina sequence data from genomic DNA of each mutant and mapped the reads to the Pgt21-0 haplotype-resolved genome assembly 2 to identify potential mutations. We first screened for single-nucleotide polymorphisms (SNPs) causing amino-acid changes in secreted protein genes, but found no genes with such mutations in more than one mutant line. Next, we looked for loss of
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