A novel locus conferring resistance to Puccinia hordei maps to the genomic region corresponding to Rph14 on barley chromosome 2HS.

Barley leaf rust (BLR), caused by Puccinia hordei, is best controlled through genetic resistance. An efficient resistance breeding program prioritizes the need to identify, characterize, and map new sources of resistance as well as understanding the effectiveness, structure, and function of resistance genes. In this study, three mapping populations were developed by crossing Israelian barley lines "AGG-396," "AGG-397," and "AGG-403" (carrying unknown leaf rust resistance) with a susceptible variety "Gus" to characterize and map resistance. Genetic analysis of phenotypic data from rust testing F3s with a P. hordei pathotype 5457 P+ revealed monogenic inheritance in all three populations. Targeted genotyping-by-sequencing of the three populations detected marker trait associations in the same genomic region on the short arm of chromosome 2H between 39 and 57 Mb (AGG-396/Gus), 44 and 64 Mb (AGG-397/Gus), and 31 and 58 Mb (AGG-403/Gus), suggesting that the resistance in all three lines is likely conferred by the same locus (tentatively designated RphAGG396). Two Kompetitive allele-specific PCR (KASP) markers, HvGBSv2-902 and HvGBSv2-932, defined a genetic distance of 3.8 cM proximal and 7.1 cM distal to RphAGG396, respectively. To increase the marker density at the RphAGG396 locus, 75 CAPS markers were designed between two flanking markers. Integration of marker data resulted in the identification of two critical recombinants and mapping RphAGG396 between markers- Mloc-28 (40.75 Mb) and Mloc-41 (41.92 Mb) narrowing the physical window to 1.17 Mb based on the Morex v2.0 reference genome assembly. To enhance map resolution, 600 F2s were genotyped with markers- Mloc-28 and Mloc-41 and nine recombinants were identified, placing the gene at a genetic distance of 0.5 and 0.2 cM between the two markers, respectively. Two annotated NLR (nucleotide-binding domain leucine-rich repeat) genes (r2.2HG0093020 and r2.2HG0093030) were identified as the best candidates for RphAGG396. A closely linked marker was developed for RphAGG396 that can be used for marker-assisted selection.

The genetic basis and interaction of genes conferring resistance to Puccinia hordei in an ICARDA barley breeding line GID 5779743.

Leaf rust of barley causes significant losses in crops of susceptible cultivars. Deploying host resistance is the most cost-effective and eco-sustainable strategy to protect the harvest. However, most known leaf rust resistance genes have been overcome by the pathogen due to the pathogen's evolution and adaptation. The discovery of novel sources of genetic resistance is vital to keep fighting against pathogen evolution. In this study, we investigated the genetic basis of resistance in barley breeding line GID 5779743 (GID) from ICARDA, found to carry high levels of seedling resistance to prevalent Australian pathotypes of Puccinia hordei. Multipathotype tests, genotyping, and marker-trait associations revealed that the resistance in GID is conferred by two independent genes. The first gene, Rph3, was detected using a linked CAPS marker and QTL analysis. The second gene was detected by QTL analysis and mapped to the same location as that of the Rph5 locus on the telomeric region of chromosome 3HS. The segregating ratio in F2 (conforming to 9 resistant: 7 susceptible genetic ratio; p > 0.8) and F3 (1 resistant: 8 segregating: 7 susceptible; p > 0.19) generations of the GID × Gus population, when challenged with pathotype 5477 P- (virulent on Rph3 and Rph5) suggested the interaction of two genes in a complementary fashion. This study demonstrated that Rph3 interacts with Rph5 or an additional locus closely linked to Rph5 (tentatively designated RphGID) in GID to produce an incompatible response when challenged with a pathotype virulent on Rph3+Rph5.

The barley leaf rust resistance gene Rph3 encodes a predicted membrane protein and is induced upon infection by avirulent pathotypes of Puccinia hordei.

Leaf rust, caused by Puccinia hordei, is an economically significant disease of barley, but only a few major resistance genes to P. hordei (Rph) have been cloned. In this study, gene Rph3 was isolated by positional cloning and confirmed by mutational analysis and transgenic complementation. The Rph3 gene, which originated from wild barley and was first introgressed into cultivated Egyptian germplasm, encodes a unique predicted transmembrane resistance protein that differs from all known plant disease resistance proteins at the amino acid sequence level. Genetic profiles of diverse accessions indicated limited genetic diversity in Rph3 in domesticated germplasm, and higher diversity in wild barley from the Eastern Mediterranean region. The Rph3 gene was expressed only in interactions with Rph3-avirulent P. hordei isolates, a phenomenon also observed for transcription activator-like effector-dependent genes known as executors conferring resistance to Xanthomonas spp. Like known transmembrane executors such as Bs3 and Xa7, heterologous expression of Rph3 in N. benthamiana induced a cell death response. The isolation of Rph3 highlights convergent evolutionary processes in diverse plant-pathogen interaction systems, where similar defence mechanisms evolved independently in monocots and dicots.

Molecular genetics of leaf rust resistance in wheat and barley.

The demand for cereal grains as a main source of energy continues to increase due to the rapid increase in world population. The leaf rust diseases of cereals cause significant yield losses, posing challenges for global food security. The deployment of resistance genes has long been considered as the most effective and sustainable way to control cereal leaf rust diseases. While genetic resistance has reduced the impact of these diseases in agriculture, losses still occur due to the ability of the respective rust pathogens to change and render resistance genes ineffective plus the slow pace at which resistance genes are discovered and characterized. This article highlights novel recently developed strategies based on advances in genome sequencing that have accelerated gene isolation by overcoming the complexity of cereal genomes. The leaf rust resistance genes cloned so far from wheat and barley belong to various protein families, including nucleotide binding site/leucine-rich repeat receptors and transporters. We review recent studies that are beginning to reveal the defense mechanisms conferred by the leaf rust resistance genes identified to date in cereals and their roles in either pattern-triggered immunity or effector-triggered immunity.

Molecular Characterization of Resistance to Soybean Rust (Phakopsora pachyrhizi Syd. & Syd.) in Soybean Cultivar DT 2000 (PI 635999).

Resistance to soybean rust (SBR), caused by Phakopsora pachyrhizi Syd. & Syd., has been identified in many soybean germplasm accessions and is conferred by either dominant or recessive genes that have been mapped to six independent loci (Rpp1 -Rpp6), but No U.S. cultivars are resistant to SBR. The cultivar DT 2000 (PI 635999) has resistance to P. pachyrhizi isolates and field populations from the United States as well as Vietnam. A F6:7 recombinant inbred line (RIL) population derived from Williams 82 × DT 2000 was used to identify genomic regions associated with resistance to SBR in the field in Ha Noi, Vietnam, and in Quincy, Florida, in 2008. Bulked segregant analysis (BSA) was conducted using the soybean single nucleotide polymorphism (SNP) USLP 1.0 panel along with simple sequence repeat (SSR) markers to detect regions of the genome associated with resistance. BSA identified four BARC_SNP markers near the Rpp3 locus on chromosome (Chr.) 6. Genetic analysis identified an additional genomic region around the Rpp4 locus on Chr. 18 that was significantly associated with variation in the area under disease progress curve (AUDPC) values and sporulation in Vietnam. Molecular markers tightly linked to the DT 2000 resistance alleles on Chrs. 6 and 18 will be useful for marker-assisted selection and backcrossing in order to pyramid these genes with other available SBR resistance genes to develop new varieties with enhanced and durable resistance to SBR.