Phenotypic and Genotypic Variation in the Interaction between Arabidopsls thaliana and Albugo Candida. Eric B. Holub . Plant Pathology and Weed Science Department, Horticulture Research International-East Mailing, West Mailing, Kent, ME19 6BJ. Edemar Brose (2), MahmutTor (2,3), Colin Clay (4), Ian R. Crute (5), and Jim L. Beynon (2). (2) Department of Biological Sciences, Wye College, University of London, Wye, Ashford, Kent, TN25 5AH, (3) Akdeniz, Universitesi, Ziraat Fakultesi, Bitki Koruma Bolumu, P.K. 510, Antalya, Turkey, (4) Department of Microbial Biotechnology, HRI-Wellesbourne, (5)Plant Pathology and Weed Science Department, HRI-Wellesbourne, Warwickshire, CV35 9EF, U.K. MPMI 8:916-928. Accepted 14 July . Copyright 1995 The American Phytopathological Society1995 The American Phytopathological Society.

Two biotrophic parasites of the wild crucifer Arabidopsis thaliana (L.) Heynh. are being used to explore the molecular basis and evolution of genotype-specific recognition and host defense. Genes for recognition of Peronospora parasitica (downy mildew) are numerous in A. thaliana and located on four of the five chromosomes as described previously. Genes for recognition of the closely related parasite Albugo Candida (white blister) are described here. In contrast to the former parasite, less than 15% of the host accessions tested were capable of recognizing either of two isolates of A. Candida. The geographic regions represented by these accessions included countries in eastern and western Europe, Asia, North America and Africa. Extensive collections from England and Germany were required to identify examples of incompatible interactions. Phenotypic variation among incompatible interactions included reduced blister formation or complete lack of asexual reproduction by the parasite. Variation in the extent of the host response was also observed. Three host genes for recognition of A. Candida (RAC), each associated with different interaction phenotypes, were identified through inheritance studies with three accessions. One of these genes at locus RACI appeared to be completely dominant, whereas the other two genes were only partially dominant or recessive under certain conditions, possibly including the effect of genetic background. One of the latter two genes defined a second locus RAC2. RACI was mapped to the top arm of chromosome 1 in the 1 cM interval between RFLP markers M254 and M253.