Incomplete Dominance of Tomato Cf Genes for Resistance to Cladosporium fulvum. Kim E. Hammond-Kosack. Sainsbury Laboratory, John Innes Centre, Colney Lane, Norwich, NR4 7UH, England. Jonathan D.G. Jones. Sainsbury Laboratory, John Innes Centre, Colney Lane, Norwich, NR4 7UH, England. MPMI 7:58-70. Accepted 27 September 1993. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1994.

Different tomato Cf resistance genes confer distinct abilities to restrict Cladosporium fulvum infections. Measurements of fungal growth revealed that their relative efficiencies decreased in the order Cf-2, Cf-5, Cf-9, Cf-4, Cf-Il, Cf-3. Plants homozygous for a given Cf gene were more effective in containing infections than when heterozygous. Cf homozygotes also responded to a two-fold lower concentration of race-specific elicitor (IF) than hetero-zygofes. The effectiveness of heterozygoles was even further reduced if produced by crosses to Lycopersicon pennellii instead of L. esculentum. Incompatibility usually occurred in the mesophyll layers and involved the gradual arrest of hyphal growth, frequent and nondichotomous hyphal branching, and a failure to form straight runner hyphae. Contained hyphae were often swollen and distorted, but those observed at the margin of the larger infections or when hyphae had been arrested within 1-2 days of entry into a substomatal cavity appeared normal. Localized host responses triggered by incompatibility included guard cell death (only in the Cf-2 containing line), enlargement of lower mesophyll cells, deposition of phenolic extracellular material on cell walls and later some cell death at the center of infections. Compatibility involved rapid colonization of the lower mesophyll apoplast by straight runner hyphae, the accumulation of highly branched mycelium in close proximity to vascular tissue in the lesion center, and finally the death of mesophyll cells directly below the sporulating conidiophores. The implications of the incomplete dominance of Cf genes, and the mechanisms by which they restrict fungal growth, are discussed.