ug99

Since 1998, when Pgt race TTKSK (Ug99) was first identified in Uganda, seven variants in the Ug99 race group have been reported in nine countries in eastern and southern Africa. Five of these variants (TTKSK, TTKST, TTTSK, PTKSK, and PTKST) have been observed in Kenya. Increased surveillance efforts in recent years have enabled detection of new virulence combinations that threaten wheat production. Three new variants in the Ug99 race group were identified from samples collected in 2013 and 2014 in Kenya. A new race, TTHST that is identical to TTKST but avirulent on Sr30 (IT 2-), was identified from a sample collected in the Central Rift Valley Region in 2013. In 2014, two new races, TTKTK and TTKTT, were identified from a total of nine samples (six collected from cv. Robin, and one from each of Eagle10, NJRBW II, and barley) in multiple regions. These two races are of special concern as both are virulent on SrTmp, a gene that is effective against all previously known races in the Ug99 group. Resistance gene SrTmp is postulated to be the source of TTKSK resistance in cv. Robin (released in 2011 in Kenya, also postulated to have Sr2) and cv. Digalu (released in 2005 in Ethiopia). The presence of new races with virulence on SrTmp may explain the high levels of stem rust severity observed in wheat cultivar Robin in Kenya in the past two years. Genotypic relationships between these new races and known races in the Ug99 race group are being characterized using SNP markers. Cultivars and elite breeding lines from Kenya, CIMMYT, and the US are being evaluated for seedling reactions to race TTKTT. With the detection of these new races, there are a total of eight variants in the Ug99 race group in Kenya.

Wheat landrace PI 177906 has seedling and field resistance to Pgt races TTKSK and TTKST. From a cross between PI 177906 and LMPG-6, 138 doubled haploid (DH) lines and 144 recombinant inbred lines (RILs) were developed and tested for seedling resistance to Pgt race TTKSK. Goodness-of-fit tests from both populations indicated that two dominant genes in PI 177906 conditioned resistance to race TTKSK. Parents and the 138 DH lines were evaluated in the field in two experiments in Kenya; one in the main season and one in the off-season. The 90K wheat iSelect SNP genotyping platform was used to genotype the parents and DH lines and data were used to construct a genetic linkage map. Two loci for seedling resistance were mapped to chromosomes 2BL and 4BL. Two major QTL for field resistance mapped to the same regions, a 14.4 cM interval on 2BL and an 8.5 cM interval on 4BL. The QTL on 2BL and 4BL explained, respectively, 31.9-32.3% and 18.2-19.1% of the variation in the off-season and 28.3-30.4% and 5.4-6.5% of the variation in the main-season. Based on the mapping results, race specificity, and the seedling infection types, the resistance gene in 2BL could be Sr28, whereas the gene on chromosome 4BL could be novel. The mapping results will be verified in the RIL population using the flanking SNP markers in KASP assays.

The shortage of stem rust resistance genes effective against the Ug99 group prompted recent efforts to increase the number of resistance genes available to breeders. We are fortunate that many new and/or cytogenetically improved rust resistance genes are now being shared with the global wheat breeding community by their developers. If we are poor stewards of these resources, the new resistance genes will eventually be defeated, and we will waste the efforts and investments that have been made. However, if we are good stewards, we should have enough resistance to achieve sustainable, durable resistance. Stewardship can be defined as the careful and responsible management of something entrusted to one’s care. What should we do to safeguard the new resistance genes? Diversification of resistance is often suggested as a way to reduce the risk of large scale epidemics. Although diversification is generally a good idea, it cannot be at the expense of leaving new genes exposed and vulnerable. A durable combination (pyramid) must be designed so that the component genes protect each other. They should reduce the probability of simultaneous pathogen mutations to virulence and they should avoid stepwise erosion of the pyramid by preventing significant reproduction of any new race that is virulent on component genes. We need pyramids to be immune or nearly immune not only to current races, but to anticipated mutants. This objective should be achievable with three or more major genes or a combination of major and minor genes. Successful gene stewardship will depend on several things. On the technical side, we will need very good markers for each gene. Each breeding program will require strong genotyping support to assemble and then validate pyramids. Most importantly, successful stewardship will require that we organize our user community to cooperate more closely. We will need to decide which genes require special stewardship and which do not. Every user of the stewardship pool resource will need to participate in earnest. It only takes one cultivar with an unprotected gene to give the pathogen a stepping stone to greater virulence. As they say, a chain is only as strong as the weakest link

Durable resistance to wheat stem rust fungus can Be achieved by developing and deploying varieties that have race-nonspecific, adult plant resistance (APR) conferred by multiple minor, slow rusting genes. Wheat lines ‘Kingbird, ‘Kiritati’, ‘Huirivis#1’, ‘Juchi’, ‘Muu’ and ‘Pavon 76’ showed high levels of APR to Ug99 races of stem rust fungus when tested in Kenya. The F5 and F6 generation recombinant inbred line (RIL) populations developed from the crosses of moderately susceptible ‘PBW343’ with five resistant parents were used in mapping. The non-Sr26 fraction of the ‘Avocet’ x Pavon 76 RIL population, developed earlier for leaf rust and stripe rust resistance studies, was also included. Field phenotyping of the parents and RILs were conducted at Njoro, Kenya for at least two years with Ug99+Sr24 (TTKST) race under high stem rust pressures. The continuous variation of APR in each RIL population and genetic analyses indicated quantitative nature of resistance that was likely governed by 3 or 4 minor genes. Single and joint year analyses by Inclusive Composite Interval Mapping (ICIM) using informative DArT and/or SSR markers identified consistent APR QTLs on chromosomes 1AL, 3BS, 5BL, 7A and 7DS in Kingbird; 2D, 3BS, 5BL and 7DS in Kiritati; 2B, 3BS, 4A, 5BL and 6B in Juchi; 2B, 3BS, 7B in Huirivis#1; 2B, 3BS and 5BL in Muu; and 1BL, 3BS, 5A and 6B in Pavon 76. QTLs on each genomic regions explained 10- 46% of the phenotypic variation for APR. Pseudo-black chaff phenotype associated with APR gene Sr2 on chromosome 3BS in all six resistant parents and identification of an APR QTL in the same region in all mapping populations confirmed the role of Sr2 in reducing stem rust severity. The 1BL QTL in Pavon 76 was in the same region where pleiotropic APR gene Lr46/Yr29/Pm39 is located. Similarly a 7DS QTL in Kingbird and Huirivis#1 was in the chromosomal region where pleiotropic APR gene Lr34/Yr18/Pm38 is located. These results indicate that the above two pleiotropic resistance genes confer APR to stem rust in addition to leaf rust, yellow rust and powdery mildew. Further studies are underway to saturate the genomic regions harboring new APR QTLs with additional molecular markers.