Abstract
AbstractInoculations with both Botrytis cinerea and Geotrichum candidum stimulated ethylene evolution in the pre‐climacteric normal tomato fruit and the non‐ripening nor mutant which did not show any rise in ethylene when uninfected. In the post‐climacteric normal fruits, new peaks in ethylene production were formed. The rise in ethylene evolution in all types of infected fruits has already been detected during the incubation period of the disease. Ethylene peaks were detected earlier and were higher in fruits infected with B. cinerea than with G. candidum, coinciding with the faster rate of growth of the former. Mechanical wounding also stimulated ethylene synthesis by the non‐ripening fruits, production being directly proportional to wound dimension. Considerably higher rates of ethylene were recorded for infected fruits than for mechanically‐injured fruits in which wound dimensions were similar to those of lesion development.Applying aminoxyacetic acid at the site of inoculation inhibited ethylene production by 55–60 % in the normal fruits and by about 80 % in the nor mutant fruits. A similar pathway of ethylene synthesis was suggested for normally ripening tomato fruit and non‐ripening infected tissues.
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