Abstract

A new postharvest hot water brushing (HWB) treatment, which sprays hot water on fruit as they move along a belt of brush‐rollers, induced resistance against green mould decay caused by Penicillium digitatum (Pers. Fr.) Sacc in ‘Star Ruby’ grapefruit. The HWB treatment (62°C for 20 s) was most effective in inducing disease resistance when the fruit were inoculated after 1 and 3 days, but was less effective when the fruit were inoculated on the same day or 7 days later. The HWB treatment induced the accumulation of a 105‐kDa protein that cross‐reacted with an antibody raised against a bovine heat shock protein 70 (HSP70) and 18‐ and 21‐kDa proteins that cross‐reacted with pea HSP18 and HSP21 antibodies. The accumulation of a grapefruit 17‐kDa protein that cross‐reacted with a pea HSP17 antibody was not affected by the HWB treatment. HWB also induced the accumulation of 21‐, 22‐ and 25‐kDa proteins that cross‐reacted with citrus and tobacco chitinase antibodies and 38‐, 42‐ and 43‐kDa proteins that cross‐reacted with citrus and tobacco β‐1,3‐glucanase antibodies. The induction of the 105‐, 18‐ and 21‐kDa HSPs by the HWB treatment indicates that it was sufficient to provide a heat stress and, thus, was able to induce biochemical changes in the fruit peel tissue. Nevertheless, the accumulation of these HSPs was probably not related to the induction of fruit resistance against P. digitatum, since their accumulation could not be induced neither by direct inoculation with the pathogen nor following exposure to other treatments, such as UV irradiation, which also induce disease resistance. On the other hand, the increases in the accumulation of the 21‐, 22‐ and 25‐kDa chitinase proteins and of the 38‐ and 43‐kDa β‐1,3‐glucanases proteins, which were observed 1 and 3 days after the HWB treatment when the fruit appeared to be more resistant to P. digitatum, may be part of the complex fruit disease resistance mechanisms induced by the heat treatment.

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