Suppression of the defence-related hydrogen peroxide burst by Penicillium digitatum during infection of citrus fruit.
D. Macarisin, M. Wisniewski and S. Droby.
Journal of Plant Pathology Volume 90 (2, Supplement) August 2008, Book of Abstract, 9th International Congress of Plant Pathology, August 24-29, 2008 Torino,Italy,. 507 pages.
2008
บทคัดย่อ
Suppression of the defence-related hydrogen peroxide burst by Penicillium digitatum during infection of citrus fruit.
Current knowledge of plant-fungal interactions postulates thata plant’s basal immune system can detect microbe-associated-molecularpatterns (MAMPs), activating a strong defence response.Pathogenic fungi, however, can counteract these defenses by suppressingsignal transduction or gene expression in plant cells, orby producing enzymes that neutralize antifungal compounds. Thepresent research shows that the postharvest pathogen,Penicilliumdigitatum,the causal agent of green mould, actively suppresses adefence-related hydrogen peroxide (H2O2) burst in citrus fruit. Incontrast, inoculation of citrus fruit with a non-pathogenic fungus,P. expansum,triggers massive production of H2O2by flavedo tissue.Both fungi induce an elevation in H2O2levels in citrus fruitexocarp from 8 to 17 h after inoculation. Thereafter,P. digitatumsuppresses H2O2production by host cells and by 66 h the H2O2level was three-fold below that in uninoculated controls. Inwound sites inoculated withP. expansum,the level of H2O2was11-fold above the control value at this time. Enzymatic removal ofH2O2by exogenous catalase, or specific suppression of H2O2productionin flavedo tissue by exogenous citric acid, significantly (P£0.05) enhanced pathogenicity ofP. digitatumand even allowednon-pathogenicP. expansumto develop lesions on lemon, orangeand grapefruit. Our results, together with recent reports suggestingthe potential involvement of citric acid and catalase in greenmould pathogenesis,indicate that in suppressing the defence-relatedhydrogen peroxide burst in citrus fruit, these compoundscould act as pathogenicity factors forP. digitatum.