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Dr. Norman Borlaug stated that rust never sleeps and this enables rust pathogens to produce new strains capable of putting rust resistance genes to rest. These pathogens continue to pose threats to global wheat production. Wheat breeders have made significant progress to control rust outbreaks using conventional selection technologies; however, some critical shifts in pathogen populations have let them down. Rapid evolution in molecular marker technologies in the last 15 years and refinement of phenomic facilities have expedited the process of discovery and characterisation of rust resistance genes to underpin the development and validation of markers closely linked with genetically diverse sources of resistance. A high proportion of the formally named rust resistance genes were characterized in the 21st century and markers closely linked with these genes have been developed and validated. The marker tagged sources of resistance to three rust diseases have equipped the wheat breeding community with tools to deploy combinations of all stage and adult plant resistance genes in future wheat cultivars. The question that whether we have enough resistance genes discovered to compete against the ever-awake rust pathogens. In our opinion, we cannot be complacent and discovery needs to continue to ensure food security. This presentation will discuss the role of advances in phenomic and genomic technologies to achieve durable rust control in wheat.
Resistance is the most economically viable approach to curb the threat of rusts in wheat. The defeat of Sr31 and vulnerability of other resistance genes to the highly virulent Pgt race Ug99 and variants led to renewed efforts to discover and deploy resistance genes/QTLs in new durably resistant varieties. Akuri is a CIMMYT-developed bread wheat line exhibiting adult plant resistance (APR) in field trials in Kenya despite susceptibility to many races at the seedling stage. This study was designed to identify genomic regions contributing APR to stem rust in Akuri. One hundred and forty one RILs and parents of an F2:5 Akuri x PBW343 population were evaluated in Njoro for APR to stem rust over three seasons. Composite interval mapping was implemented on Windows QTL Cartographer to detect QTLs at a LOD threshold of 2.5 utilizing 910 high quality SNPs previously typed on the DArT-GBS platform. Preliminary QTL analyses revealed loci on chromosomes 1B, 2B and 3B consistently contributing to stem rust resistance. These QTL respectively explained ~7, 9, and 8% of the phenotypic variation. A comparison with the recently reported QTL consensus map revealed that the QTL herein discovered are probably novel. Work is underway to saturate the identified genomic regions with microsatellite markers to identify candidate, linked markers for use in marker assisted selection (MAS)
Stripe rust of wheat, caused by Puccinia striiformis f. sp. tritici (Pst), is a major threat to global food security. Although stripe rust was detected for the first time in Eastern Australia in 1979, Western Australia (WA) remained free from stripe rust until 2002. The Pst incursion in WA was pathotyped as 134 E16A+ and differed from the most widely virulent pre-2002 group by combined virulence to Yr8 and Yr9 and avirulence for Yr3 and Yr4. An advanced breeding line, WAWHT2046, expressed resistant to moderately resistant (R-MR) response to 134 E16A+ under field conditions, and infection type (IT) 23C - 3C at the seedling stage. The resistance gene Yr34 that controlled stripe rust in WAWHT2046 was 12.2 cM distal to the awn inhibitor B1 in chromosome 5AL (Bariana et al. 2006; Theor Appl Genet 112:1143-1148) based on a Carnamah/WAWHT2046 doubled haploid (DH) population. The present investigation was planned to identify SNP markers closely linked with Yr34. Eight homozygous resistant and eight homozygous susceptible lines from the Carnamah/WAWHT2046 DH population were used for selective genotyping using SNP markers. Twenty four SNP markers were associated with resistance. Kompetitive allele-specific primers (KASP) were designed and SNP markers were genotyped on the DH population. SNP marker IWB80451 mapped 1.7 cM proximal to Yr34.