Uromyces appendiculatus in Honduras: Pathogen Diversity and Host Resistance Screening

Acevedo, M., Steadman, J. R., and Rosas, J. C. 2013. Uromyces appendiculatus in Honduras: Pathogen diversity and host resistance screening. Plant Dis. 97:652-661. Bean rust, caused by the fungus Uromyces appendiculatus, is a major constraint for common bean production worldwide. Virulence of U. appendiculatus collected from wild and cultivated Phaseolus spp. was examined in 28 locations across Honduras. Host accessions representing wild and domesticated Phaseolus spp. collected at the same sampling locations were evaluated for resistance against U. appendiculatus. In total, 91 pathotypes were identified from 385 U. appendiculatus isolates according to their virulence on each of the 12 host differentials. No significant difference in pathogen total virulence, measured as the mean disease score, was found between locations. However, significant differences were found in pathotype virulence among isolates collected from different Phaseolus spp. within a location. Moreover, when locations were compared on the basis of pathotype occurrence and frequency, differences among locations were evident. No two locations had the same pathotype composition. The most common pathotype was virulent on 9 of the 12 differential lines. A high number of resistant accessions were identified in Phaseolus coccineus and P. lunatus. Although most wild P. vulgaris accessions were highly susceptible, rust resistance was observed in P. vulgaris landraces collected from farmer’s fields. Thirty-two (52%) of the accessions screened showed intermediate to high levels of resistance and, of those, 16% were P. coccineus accessions. Our findings support the hypothesis that interaction of U. appendiculatus in host populations composed of diverse Phaseolus spp. and genotypes has favored highly diverse and virulent pathotypes, creating a center for virulence diversity of the pathogen in Honduras. The high percentage of intermediate and highly resistant accessions identified in the present study supports the strategy of collecting plants from the center of diversity of a pathogen or in locations with high incidence of disease and pathogen diversity to maximize the probability of identifying new sources of resistance. Bean rust, caused by the fungus Uromyces appendiculatus, is a major constraint for common bean production around the world. U. appendiculatus epidemics have been most serious in tropical and subtropical areas in the Americas and Africa but severe epidemics have also occurred in temperate climates. A high virulence diversity in U. appendiculatus in many geographic regions has been documented (14,21,23,33,39,40,41,44). Despite the high number of virulence patterns described worldwide, two major pathotype groups can be distinguished in U. appendiculatus. One of the pathotype groups is virulent on common bean cultivars of Andean origin while the second pathotype group is virulent on common bean cultivars of both the Andean gene pool and the Middle American gene pool (2,23). Based on these results, parallel evolution of host and pathogen has been suggested. Disease resistance is the least expensive and easiest management strategy in most common bean production systems, especially in developing countries where common bean crops are mainly produced by small-scale farmers (24). However, the high pathogenic and genetic variability of the common bean rust fungus has challenged the development of resistant varieties. This challenge is enhanced in the tropics, where multiple common-bean-growing seasons occur in a single year and a conducive environment and adequate moisture favor the development of rust epidemics and pathogen diversity. Many rust resistance genes have been identified using specific pathotypes of the bean rust pathogen. These genes include Ur-3, Ur-4, Ur-5, Ur-6, Ur-7, Ur-9/Ur-12, Ur-11, Ur-13 Ur-Ouro Negro, and Ur-Resisto. Other sources of resistance have been identified in bean cultivars and lines but the inheritance of the resistance is not fully understood or has yet to be determined (see Liebenberg et al. [15] for an inclusive list of the sources of rust resistance and their origin). Despite the availability of many sources of resistance to bean rust pathotypes or physiological races, none of these sources are effective against all races. Gene pyramiding or stacking has been used effectively to produce bean cultivars with multiple rust resistances in several bean market classes (29,30,42,43,45). Rust diversity studies have shown high virulence and pathogenic diversity in Honduras (2,14). However, no specific cultivars or lines have been developed that are resistant to U. appendiculatus populations in Honduras. An understanding of pathogen virulence variability in natural host populations can provide insights into the evolution of pathogen virulence, aid the search for new sources of resistance, and guide resistance gene deployment. Based on the challenge that high virulence diversity represents for breeding rustresistant bean cultivars, especially for Honduras, sources of rust resistance need to be identified to ensure broader and durable resistance in common bean cultivars for the Honduran market. Thus, the objectives of this study were to (i) characterize the virulence diversity of U. appendiculatus collected from wild and domesticated populations of Phaseolus spp. in geographically diverse areas of Honduras, (ii) collect and screen Honduran wild and domesticated Phaseolus spp. for rust resistance, and (iii) assess the importance of the occurrence of domesticated and wild Phaseolus spp. in Honduras on U. appendiculatus virulence diversity throughout the country. Materials and Methods Pathogen origin. Collection areas for U. appendiculatus urediniospores and Phaseolus spp. seed in Honduras were selected based on the wild bean climate probability GIS-model-based map developed by the International Center of Tropical Agriculture (3) and bean production regions in Honduras. Seed of the landraces Corresponding author: M. Acevedo, E-mail: [email protected] Accepted for publication 12 October 2012. http://dx.doi.org/10.1094 / PDIS-02-12-0169-RE © 2013 The American Phytopathological Society