IN A PAPER (Boone et al., 1957) published concurrently with this, references are given to earlier papers in this series on the genetics, nutrition, and pathogenicity of Venturia inaequalis (Cke.) Wint., and the pathogenicity of many induced biochemical mutants is reported. Mutants requiring, respectively, biotin, nicotinic acid, pantothenic acid, inositol, or reduced sulfur were pathogenic like the wild-type line from which they were derived. Mutants requiring choline, riboflavin, purines, pyrimidines, arginine, histidine, methionine, or proline were nonpathogenic. Three lines of evidence indicated that the losses of pathogenicity were due to the nutritional deficiencies: (1) loss of pathogenicity was associated with auxotrophy, (2) mutants with like nutritional requirements showed like losses of pathogenicity, (3) all mutant progeny from crosses of nonpathogenic mutants with wild type were nonpathogenic whereas all wild-type progeny from the same crosses were pathogenic. It was hypothesized that if the mutants were nonpathogenic because they were nutritionally deficient, they should become pathogenic2 if their required substances were made available to them during the incubation period. This paper reports studies made to test this hypothesis. An account of the growth of the mutants in vitro in leaf sap is also given. Preliminary reports have been made (Boone et al., 1954; Keitt and Boone, 1955, 1956; Kline, 1956; Kline et al., 1956). MATERIALS AND METHODS.-Mutants employed.All mutants used in this study were derived from the monoascosporic, highly pathogenic, wild-type line 365-4 (Boone et al., 1956). The attempts at restoring pathogenicity were made mainly with eight mutants that had been found to be nonpathogenic in previous studies (Keitt and Boone, 1954; Boone et al., 19,57). The mutants required, respec-