Tumor formation in Vitis species and hybrids, incited by Agrobacterium tumefaciens, was altered by chemical, physical, developmental, and genetic variables. Knowledge of the effect of these variables was used to develop a stringent in vitro assay system to select parents for a study of genetic factors that modulate tumor formation. Tumor formation was reduced by short day preconditioning of assay plants and by inoculation of the morphological apex of isolated stem segments. Pretreatment of plants with auxin or cytokinin altered specificity in various combinations of strains and host genotypes. All Vitis species and hybrids formed tumors in response to strains designated as limited host range, but some displayed a necrotic reaction (cell death at and below site of inoculation) or a null response (same as the response to inoculation with an avirulent strain) to strains designated as wide host range (VC Knauf, CG Panagopoulos, EW Nester [1982] Phytopathology 72: 1545-1549). Screens of F1 progeny, derived from crosses of null, necrotic, and tumor-producing phenotypes, demonstrated that the null and the necrotic phenotypes were modulated by dominant and recessive host genes. The extent of cellular necrosis in the necrotic phenotype was modified by the morphological location of the inoculation site, by the presence of buds on the host stem, and by deletion of the tryptophane monooxygenase locus gene of the Ti-plasmid.The tumor-inducing plasmid ofAgrobacterium tumefaciens contains two regions, termed the virulence (vir) and tumorinducing DNA (T-DNA), that coordinately participate in the excision of DNA from the pathogen and its transfer into the host genome (11,17). The current model for infection of host cells by Agrobacterium predicts that phenolic metabolites produced by wounded plant cells activate plasmid vir genes of the bacterium (22). Once activated, the genes modulate the excision and packaging of T-DNA and facilitate its transfer into the host plant genome (17,22). Expression of T-DNA in host cells alters the endogenous levels of auxin, cytokinin, and ethylene (6,11,17), which results in the loss of cellular totipotency (11,17 3,17,27). Bacterial host range and virulence determinants have been attributed to structural and organizational differences in T-DNA loci (1,17,21,(27)(28)(29)30) and to structural differences in at least two vir loci (30,31). Some investigators suggest that chromosomal loci might also modulate host selectivity (17,25). The role of the host genome in Agrobacterium-host compatibility has not received as much consideration as that of the pathogen. However, intergeneric (3,12,25,26,29,30) and intraspecific and cultivar variations (1, 2, 7-9, 19, 23, 24, 27) in hostresponse to WHR and/or LHR strains have been reported. A preliminary analysis of Vitis hybrids showed that resistance to A. tumefaciens was a heritable trait (23).The primary goal of our research was to develop a system to study the interactions of bacterial virulence genes and host genes so that the molecular and bioch...