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Two classes of genes are used for breeding rust resistant wheat. The first class, called R (for resistance) genes, are pathogen race specific in their action, effective at all plant growth stages and probably mostly encode immune receptors of the nucleotide binding leucine rich repeat (NB-LRR) class. The second class is called adult plant resistance genes (APR) because resistance is usually functional only in adult plants, and, in contrast to most R genes, the levels of resistance conferred by single APR genes are only partial and allow considerable disease development. Some but not all APR genes provide resistance to all isolates of a rust pathogen species and a subclass of these provides resistance to several fungal pathogen species. Initial indications are that APR genes encode a more heterogeneous range of proteins than R proteins. Two APR genes, Lr34 and Yr36, have been cloned from wheat and their products are an ABC transporter and a protein kinase, respectively. Lr34 and Sr2 have provided long lasting and widely used (durable) partial resistance and are mainly used in conjunction with other R and APR genes to obtain adequate rust resistance. We caution that some APR genes indeed include race specific, weak R genes which may be of the NB-LRR class. A research priority to better inform rust resistance breeding is to characterize further APR genes in wheat and to understand how they function and how they interact when multiple APR and R genes are stacked in a single genotype by conventional and GM breeding. An important message is do not be complacent about the general durability of all APR genes.

[...]new variants of Asian soybean rust (Phakopsora pachyrhizi) detected in Brazil and the United States pose a major constraint to soybean cultivation [2]. Since genetic resistance can provide effective and chemical-free disease control, many efforts are directed towards isolating rust-resistance genes in crop plants and understanding how to best deploy them for durable resistance [3]. [...]the stripe rust-resistance gene Yr36 encodes a chloroplast-localised protein with kinase and steroidogenic acute regulatory protein-related transfer (START) lipid-binding domains and is proposed to reduce the detoxification of reactive oxygen species by phosphorylation of a thylakoid-associated ascorbate peroxidase, resulting in enhanced defense responses [18]. Transgenic expression of the wheat Lr34 or Lr67 genes in other cereal species, such as durum wheat, barley, rice, and maize, confers resistance to multiple adapted pathogens of these crops, suggesting that the roles of these genes in infection are conserved across a wide taxonomic range [22]. [...]these genes have the potential to be used as new sources of basal/background resistance in other species, although it remains to be determined whether they can function in eudicots. Basal immunity would be relatively more important in interactions where the nonhost species is distantly related to the normal host, and NLR immunity more important in interactions involving a more closely related nonhost species. [...]it is not surprising that many responses associated with NHR overlap those activated during host resistance [4, 27, 28, 29].

The re-emergence of stem rust on wheat in Europe and Africa is reinforcing the ongoing need for durable resistance gene deployment. Here, we isolate from wheat, Sr26 and Sr61 , with both genes independently introduced as alien chromosome introgressions from tall wheat grass ( Thinopyrum ponticum ). Mutational genomics and targeted exome capture identify Sr26 and Sr61 as separate single genes that encode unrelated (34.8%) nucleotide binding site leucine rich repeat proteins. Sr26 and Sr61 are each validated by transgenic complementation using endogenous and/or heterologous promoter sequences. Sr61 orthologs are absent from current Thinopyrum elongatum and wheat pan genome sequences, contrasting with Sr26 where homologues are present. Using gene-specific markers, we validate the presence of both genes on a single recombinant alien segment developed in wheat. The co-location of these genes on a small non-recombinogenic segment simplifies their deployment as a gene stack and potentially enhances their resistance durability. The tall wheat grass-derived stem rust resistance genes Sr26 and Sr61 are among a few ones that are effective to all current dominant races of stem rust, including Ug99. Here, the authors show that the two genes are present in a small non-recombinogenic segment but encode two unrelated NLR proteins.

A method for rapid cloning of plant disease-resistance genes could provide sustainable, genetic solutions to crop pests and pathogens in place of agrichemicals. Wild relatives of domesticated crop species harbor multiple, diverse, disease resistance (R) genes that could be used to engineer sustainable disease control. However, breeding R genes into crop lines often requires long breeding timelines of 5–15 years to break linkage between R genes and deleterious alleles (linkage drag). Further, when R genes are bred one at a time into crop lines, the protection that they confer is often overcome within a few seasons by pathogen evolution 1 . If several cloned R genes were available, it would be possible to pyramid R genes 2 in a crop, which might provide more durable resistance 1 . We describe a three-step method (MutRenSeq)-that combines chemical mutagenesis with exome capture and sequencing for rapid R gene cloning. We applied MutRenSeq to clone stem rust resistance genes Sr22 and Sr45 from hexaploid bread wheat. MutRenSeq can be applied to other commercially relevant crops and their relatives, including, for example, pea, bean, barley, oat, rye, rice and maize.

Bread wheat ( Triticum aestivum ) is a globally dominant crop and major source of calories and proteins for the human diet. Compared with its wild ancestors, modern bread wheat shows lower genetic diversity, caused by polyploidisation, domestication and breeding bottlenecks 1 , 2 . Wild wheat relatives represent genetic reservoirs, and harbour diversity and beneficial alleles that have not been incorporated into bread wheat. Here we establish and analyse extensive genome resources for Tausch’s goatgrass ( Aegilops tauschii ), the donor of the bread wheat D genome. Our analysis of 46 Ae. tauschii genomes enabled us to clone a disease resistance gene and perform haplotype analysis across a complex disease resistance locus, allowing us to discern alleles from paralogous gene copies. We also reveal the complex genetic composition and history of the bread wheat D genome, which involves contributions from genetically and geographically discrete Ae. tauschii subpopulations. Together, our results reveal the complex history of the bread wheat D genome and demonstrate the potential of wild relatives in crop improvement. Analysis of 46 newly sequenced or re-sequenced Tausch’s goatgrass ( Aegilops tauschii ) accessions establishes the origin of the bread wheat ( Triticum aestivum ) D genome from genetically and geographically discrete Ae. tauschii subpopulations.

Agricultural crops benefit from resistance to pathogens that endures over years and generations of both pest and crop. Durable disease resistance, which may be partial or complete, can be controlled by several genes. Some of the most devastating fungal pathogens in wheat are leaf rust, stripe rust, and powdery mildew. The wheat gene Lr34 has supported resistance to these pathogens for more than 50 years. Lr34 is now shared by wheat cultivars around the world. Here, we show that the LR34 protein resembles adenosine triphosphate-binding cassette transporters of the pleiotropic drug resistance subfamily. Alleles of Lr34 conferring resistance or susceptibility differ by three genetic polymorphisms. The Lr34 gene, which functions in the adult plant, stimulates senescence-like processes in the flag leaf tips and edges.

Plants possess intracellular immune receptors designated “nucleotide-binding domain and leucine-rich repeat” (NLR) proteins that translate pathogen-specific recognition into disease-resistance signaling. The wheat immune receptors Sr33 and Sr50 belong to the class of coiled-coil (CC) NLRs. They confer resistance against a broad spectrum of field isolates of Puccinia graminis f. sp. tritici, including the Ug99 lineage, and are homologs of the barley powdery mildew-resistance protein MLA10. Here, we show that, similarly to MLA10, the Sr33 and Sr50 CC domains are sufficient to induce cell death in Nicotiana benthamiana. Autoactive CC domains and full-length Sr33 and Sr50 proteins self-associate in planta. In contrast, truncated CC domains equivalent in size to an MLA10 fragment for which a crystal structure was previously determined fail to induce cell death and do not self-associate. Mutations in the truncated region also abolish self-association and cell-death signaling. Analysis of Sr33 and Sr50 CC domains fused to YFP and either nuclear localization or nuclear export signals in N. benthamiana showed that cell-death induction occurs in the cytosol. In stable transgenic wheat plants, full-length Sr33 proteins targeted to the cytosol provided rust resistance, whereas nuclear-targeted Sr33 was not functional. These data are consistent with CC-mediated induction of both cell-death signaling and stem rust resistance in the cytosolic compartment, whereas previous research had suggested that MLA10-mediated cell-death and disease resistance signaling occur independently, in the cytosol and nucleus, respectively.

The common wheat cultivar Parula possesses a high level of slow rusting, adult plant resistance (APR) to all three rust diseases of wheat. Previous mapping studies using an Avocet-YrA/Parula recombinant inbred line (RIL) population showed that APR to leaf rust (Puccinia triticina) in Parula is governed by at least three independent slow rusting resistance genes: Lr34 on 7DS, Lr46 on 1BL, and a previously unknown gene on 7BL. The use of field rust reaction and flanking markers identified two F6 RILs, Arula1 and Arula2, from the above population that lacked Lr34 and Lr46 but carried the leaf rust resistance gene in 7BL, hereby designated Lr68. Arula1 and Arula2 were crossed with Apav, a highly susceptible line from the cross Avocet-YrA/Pavon 76, and 396 F4-derived F5 RILs were developed for mapping Lr68. The RILs were phenotyped for leaf rust resistance for over 2 years in Ciudad Obregon, Mexico, with a mixture of P. triticina races MBJ/SP and MCJ/SP. Close genetic linkages with several DNA markers on 7BL were established using 367 RILs; Psy1-1 and gwm146 flanked Lr68 and were estimated at 0.5 and 0.6 cM, respectively. The relationship between Lr68 and the race-specific seedling resistance gene Lr14b, located in the same region and present in Parula, Arula1 and Arula2, was investigated by evaluating the RILs with Lr14b-avirulent P. triticina race TCT/QB in the greenhouse. Although Lr14b and Lr68 homozygous recombinants in repulsion were not identified in RILs, γ-irradiation-induced deletion stocks that lacked Lr68 but possessed Lr14b showed that Lr68 and Lr14b are different loci. Flanking DNA markers that are tightly linked to Lr68 in a wide array of genotypes can be utilized for selection of APR to leaf rust.

The locus Lr34/Yr18/Pm38 confers partial and durable resistance against the devastating fungal pathogens leaf rust, stripe rust, and powdery mildew. In previous studies, this broad-spectrum resistance was shown to be controlled by a single gene which encodes a putative ATP-binding cassette transporter. Alleles of resistant and susceptible cultivars differed by only three sequence polymorphisms and the same resistance haplotype was found in the three independent breeding lineages of Lr34/Yr18/Pm38. Hence, we used these conserved sequence polymorphisms as templates to develop diagnostic molecular markers that will assist selection for durable multi-pathogen resistance in breeding programs. Five allele-specific markers (cssfr1-cssfr5) were developed based on a 3 bp deletion in exon 11 of the Lr34-gene, and one marker (cssfr6) was derived from a single nucleotide polymorphism in exon 12. Validation of reference genotypes, well characterized for the presence or absence of the Lr34/Yr18/Pm38 resistance locus, demonstrated perfect diagnostic values for the newly developed markers. By testing the new markers on a larger set of wheat cultivars, a third Lr34 haplotype, not described so far, was discovered in some European winter wheat and spelt material. Some cultivars with uncertain Lr34 status were re-assessed using the newly derived markers. Unambiguous identification of the Lr34 gene aided by the new markers has revealed that some wheat cultivars incorrectly postulated as having Lr34 may possess as yet uncharacterised loci for adult plant leaf and stripe rust resistance.

Plants respond to pathogen infection by relocalizing sugar from bacterial colonization sites Plants are energy storage factories. Photosynthetic cells convert energy from sunlight to sugars that are transported to growing tissues via both extracellular and intercellular trafficking pathways. Many pathogens have evolved mechanisms to infect the nutrient-rich niche of plant tissues and exploit these sugar pipelines. Some pathogens manipulate sugar transport to enhance their access to carbohydrate. For example, Xanthomonas bacteria deliver transcriptionactivator–like effector proteins into leaf cells. These proteins induce expression of SWEET family sugar transporters to release sucrose into the apoplastic (extracellular) space where the bacteria grow ( 1 ). On page 1427 of this issue, Yamada et al. ( 2 ) show that, in return, plants can also regulate sugar transporters, to redistribute the sugars away from the infection niche, removing the pathogens' energy source and limiting their proliferation.