|Droby, S - ARO, ISRAEL|
|Cohen, L - ARO, ISRAEL|
|Rafael, G - ARO, ISRAEL|
Submitted to: Postharvest International Symposium Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: March 15, 2009
Publication Date: April 1, 2009
Citation: Wisniewski, M.E., Macarisin, D., Droby, S., Cohen, L., Rafael, G. 2009. Elucidation of the biochemical basis of specificity and pathogenicity of Penicillium digitatum on citrus fruit. Postharvest International Symposium Proceedings. p. 114. Technical Abstract: Green mold caused by Penicillium digitatum is the most damaging postharvest diseases of citrus fruit. This Penicillium species is specific to citrus fruit and do not cause progressive decay in any other fresh fruit or vegetable crops. While the etiology of P. digitatum is well understood, the physiological and biochemical basis of its host specificity is much less clear. In this work, we report that volatiles emitted from wounded peel tissue play a major role in the recognition and initial stages of spore germination of P. digitatum. Volatiles of various citrus cultivars had a pronounced stimulatory effect on germination and germ tube elongation. When exposed to volatiles from grapefruit, the percentage of germinated spores of P. digitatum was 10 fold n as compared to the control. In contrast, Botrytis cinerea and Penicillium expansum were either not affected or inhibited by the peel volatiles. GS-MS analysis of volatiles present in the peel of various citrus fruit cultivars revealed that limonene is the major fruit peel volatile. Following germination and before colonization of fruit tissue, P. digitatum needs to overcome defense mechanisms in the peel. Our findings suggest that in order to cause decay, P. digitatum actively suppresses a defense-related hydrogen peroxide H(2)O(2) burst in citrus fruit. In contrast, inoculation of citrus fruit with a non-pathogenic fungus, Penicillium expansum, triggers massive production of H(2)O(2) by flavedo tissue. Both fungi induce an elevation in H(2)O(2) levels in citrus fruit exocarp from 8 to 17 h after inoculation. Thereafter, P. digitatum suppresses H(2)O(2) production by host cells and by 66 h the H(2)O(2) level was three-fold below that in non-inoculated controls. In wound sites inoculated with P. expansum, the level of H(2)O(2) was 11-fold above the control value at this time point. Enzymatic removal of H(2)O(2) by exogenous catalase or specific suppression of H(2)O(2) production in flavedo tissue by exogenous citric acid significantly (P = 0.05) enhanced pathogenicity of P. digitatum and even allowed non-pathogenic P. expansum to develop lesions on lemon, orange, and grapefruit. These results, together with recent reports suggesting the potential involvement of citric acid and catalase in green mold pathogenesis, indicate that suppression of the defense-related hydrogen peroxide burst in citrus fruit by these compounds could act as pathogenicity factors for P. digitatum on citrus fruit.