Wheat stripe rust, caused by Puccinia striiformis f. sp. tritici, is most destructive in the western United States and has become increasingly important in the south-central states. The disease has been monitored by collaborators through field surveys and in disease nurseries throughout the United States. In the year 2000, stripe rust occurred in more than 20 states throughout the country, which was the most widespread occurrence in recorded history. Although fungicide applications in many states reduced yield losses, the disease caused multimillion dollar losses in the United States, especially in Arkansas and California. One of the prevalent cultivars, RSI 5, had a yield loss of about 50% in the Sacramento-San Joaquin Delta region of California. In the Pacific Northwest, wheat losses due to stripe rust were minimal because cultivars with durable resistance were widely grown and the weather in May 2000 was not favorable for the disease. To identify races of the pathogen, stripe rust collections from 20 states across the United States were analyzed on 20 wheat differential cultivars, including Clement (Yr9, YrCle), Compair (Yr8, Yr19), and the Yr8 and Yr9 near-isogenic lines. In 2000, 21 previously identified races and 21 new races were identified. Of the 21 new races, 8 were pathotypes with combinations of virulences previously known to exist in the United States, and 13 had virulences to one or more of the lines Yr8, Yr9, Clement, or Compair. This is the first report of virulence to Yr8 and Yr9 in the United States. Most of the new races were also virulent on Express. Races that are virulent on Express have been identified in California since 1998. The races virulent on Yr8, Yr9, and Express were widely distributed in California and states east of the Rocky Mountains in 2000. The epidemic in 2000 demonstrates that increased efforts to breed for stripe rust resistance are needed in California, the south-central states, and some other states in the Great Plains. Diversification of resistance genes and use of durable resistance should prevent large-scale and severe epidemics.

Several new races of the stripe rust pathogen have become frequent throughout the wheat growing regions of the United States since 2000. These new races are virulent to most of the wheat seedling resistance genes limiting the resistance sources that can be used to combat this pathogen. High-temperature adult-plant (HTAP) stripe rust resistance has proven to be more durable than seedling resistance due to its non-racespecific nature, but its use is limited by the lack of mapping information. We report here the identification of a new HTAP resistance gene from Triticum turgidum ssp. dicoccoides (DIC) designated as Yr36. Lines carrying this gene were susceptible to almost all the stripe rust pathogen races tested at the seedling stage but showed adult-plant resistance to the prevalent races in California when tested at high diurnal temperatures. Isogenic lines for this gene were developed by six backcross generations. Field tests in two locations showed increased levels of field resistance to stripe rust and increased yields in isogenic lines carrying the Yr36 gene compared to those without the gene. Recombinant substitution lines of chromosome 6B from DIC in the isogenic background of durum cv. Langdon were used to map the Yr36 gene on the short arm of chromosome 6B completely linked to Xbarc101, and within a 2-cM interval defined by PCR-based markers Xucw71 and Xbarc136. Flanking locus Xucw71 is also closely linked to the grain protein content locus Gpc-B1 (0.3-cM). Marker-assisted selection strategies are presented to improve stripe rust resistance and simultaneously select for high or low Gpc-B1 alleles.

Deletion or alteration of an avirulence gene are two mechanisms that allow pathogens to escape recognition mediated by the corresponding resistance gene in the host. We studied these two mechanisms for the NIP1 avirulence gene in field populations of the fungal barley pathogen Rhynchosporium secalis. The product of the avirulence gene, NIP1, causes leaf necrosis and elicits a defense response on plants with the Rrs1 resistance gene. A high NIP1 deletion frequency (45%) was found among 614 isolates from different geographic populations on four continents. NIP1 was also sequenced for 196 isolates, to identify DNA polymorphisms and corresponding NIP1 types. Positive diversifying selection was found to act on NIP1. A total of 14 NIP1 types were found, 11 of which had not been described previously. The virulence of the NIP1 types was tested on Rrs1 and rrs1 barley lines. Isolates carrying three of these types were virulent on the Rrs1 cultivar. One type each was found in California, Western Europe, and Jordan. Additionally, a field experiment with one pair of near-isogenic lines was conducted to study the selection pressure imposed by Rrs1 on field populations of R. secalis. Deletion of NIP1 was the only mechanism used to infect the Rrs1 cultivar in the field experiment. In this first comprehensive study on the population genetics of a fungal avirulence gene, virulence to Rrs1 in R. secalis was commonly achieved through deletion of the NIP1 avirulence gene but rarely also through point mutations in NIP1.

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