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Reference Report for SoyBase10189514819
Title:Phytophthora sojae races have arisen by clonal evolution and by rare outcrosses.
Authors:Foerster, H., Tyler, B.M., Coffey, M.D.
Source:Mol. Plant Microb. Interact. 1994, 7(6):780-791
Abstract:An extensive set of nuclear and mitochondrial restriction fragment length polymorphisms (RFLPs) was used to examine the genetic relationships among 48 isolates of Phytophthora sojae, an oomycete pathogen of soybean. This organism is diploid and homothallic. The isolates examined encompassed 25 physiological races of the pathogen, including races 36 and 37 which we describe here for the first time. The results reveal a moderate degree of diversity within the species; about 18% of all detected nuclear restriction fragments were polymorphic in at least one isolate. One group of isolates, representing seven physiological races, had RFLPs nearly identical to isolates of the first described race, race 1, and probably arose from race 1 isolates clonally by mutation. There was much more genetic variation among the remaining isolates. The distribution of RFLP alleles among these isolates suggests most of the genetic variation in the species is found in four genotypes (progenitor lines) represented by isolates P1658 (race 1), P7064 (race 7), P7074 (race 17), and P7076 (race 19), respectively. All the other isolates appear to have been produced by rare outcrosses between representatives of these four genotypes. The distribution of avirulence phenotypes against Rps genes (soybean resistance genes against P. sojae) is consistent with the reassortment of single avirulence genes as a result of the same outcrosses. Therefore it is proposed that occasional outcrosses have been a major contributor to the origin of new physiological races of P. sojae, in addition to clonal evolution. In concordance with these mechanisms, no correlation was observed between particular RFLPs and race types. Thus it will be very difficult to use RFLP or RAPD markers to directly identify race types of new field isolates unless the markers are derived directly from avirulence genes.






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