Root colonization of tomato cultivars susceptible or resistant to Fusarium crown and root rot disease, caused by the pathogen Fusarium oxysporum f.sp. radicis-lycopersici Jarvis & Shoemaker, was studied histologically. In seedlings of susceptible cultivars ('Ohio MR13', 'Bonny Best', and 'Vendor') held at 22 °C, direct penetration of epidermal cells occurred by 24 h after inoculation and colonization of suberized hypodermal cells and adjacent intercellular spaces by 72 h. The cortex was colonized between 72 and 96 h after inoculation and the stele was commonly colonized by 120 to 144 h. Colonization of the cortex and stele was associated with the breakdown of parenchymatous cell walls and middle lamellae near fungal hyphae. In cultivars resistant by a single dominant gene ('CR6', 'Larma', and 'B82-865') colonization was similar to that in susceptible cultivars until 72 h after inoculation. By this time, papillae were abundant within hypodermal cells. Successful colonization of hypodermal sites was associated with the incorporation of phenolic or lignin-like materials and suberin within cell walls of the underlying cortex. These cortical wall modifications were paralleled by the deposition of electron-opaque material into cortical cell walls and middle lamellae and the production of finely granular bands around the peripheries of colonized intercellular spaces. Phenolic-containing structural defensive barriers (i.e., papillae and modified cortical cell walls) appear to be important in limiting fungal colonization in cultivars possessing single dominant gene resistance to this disease.

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Colonization of root tissues in tomato seedlings genetically resistant to Fusarium oxysporum f.sp. radicis-lycopersici Jarvis & Shoemaker occurred following exposure to a sublethal concentration of the herbicide glyphosate (1.0 mM for 24 h prior to inoculation). The glyphosate-induced colonization was associated with an inefficiency in incorporation of phenolic materials into the papillae and into the modified cortical cell walls normally formed in response to this pathogen. Glyphosate-induced susceptibility decreased when the glyphosate was applied at 24 or 48 h after inoculation. Plants supplied with exogenous L-phenylalanine failed to exhibit reduced susceptibility after glyphosate exposure. In radial growth bioassays, growth of the fungus was unaffected by 4.0 mM glyphosate. α-Aminooxyacetic acid, an inhibitor of phenylalanine ammonia lyase, also increased the severity of the disease in resistant plants. Glyphosate also induced susceptibility to an isolate of F. solani f.sp. pisi, which was normally not pathogenic to tomato.

Sixteen sweet corn cultivars, representing a range of endosperm genotypes, were evaluated to determine cultivar tolerance to nicosulfuron plus rimsulfuron in greenhouse and field studies conducted over a two-year period. Response to nicosulfuron plus rimsulfuron varied widely, depending on cultivar and application rate. In the field, four cultivars were tolerant to applications of nicosulfuron plus rimsulfuron at rates of 50 g/ha. In the greenhouse, eight cultivars were tolerant to nicosulfuron plus rimsulfuron at 25 g/ha. ‘Merit’ and ‘Silver Extra Sweet’ were most sensitive, with applications of nicosulfuron plus rimsulfuron resulting in death of all plants. ‘Miracle,’ ‘Extra Early Super Sweet,’ ‘Bunker Hill,’ and ‘Sweet Belle’ were tolerant.