Macarisin, D., U.S. Department of Agriculture-Agricultural Research Service (USDA-ARS), Appalachian Fruit Research Station, 2217 Wiltshire Road, Kearneysville, WV 25430, United States
Cohen, L., Department of Postharvest Science of Fresh Produce, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel
Eick, A., Department of Postharvest Science of Fresh Produce, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel
Rafael, G., Department of Postharvest Science of Fresh Produce, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel
Belausov, E., Department of Postharvest Science of Fresh Produce, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel
Wisniewski, M., U.S. Department of Agriculture-Agricultural Research Service (USDA-ARS), Appalachian Fruit Research Station, 2217 Wiltshire Road, Kearneysville, WV 25430, United States
Droby, S., Department of Postharvest Science of Fresh Produce, Agricultural Research Organization, Volcani Center, Bet Dagan 50250, Israel

During the infection of citrus fruit by Penicillium digitatum there is little evidence of a host defense response. This suggests that P. digitatum has the ability to suppress host defenses. The current study demonstrates that P. digitatum suppresses a defense-related hydrogen peroxide (H2O 2) burst in host tissue. In contrast, the nonhost pathogen, Penicillium expansum, triggers production of a significant amount of H 2O2 in citrus fruit exocarp. Using laser scanning confocal microscopy, we demonstrated that P. digitatum suppressed an elevation in H 2O2 up to 42 h after inoculation. Nevertheless, H 2O2 levels around wounds inoculated with P. expansum increased by 63-fold above the control. P. digitatum continued to suppress H2O2 production in citrus fruit exocarp up to 66 h postinoculation and H2O2 levels were actually threefold below that of noninoculated controls. In contrast, the H2O 2 level was still about 11-fold above the control value in wound sites inoculated with P. expansum. Studies on the effect of organic acids (as pH modulators) on the response of citrus fruit to compatible and noncompatible pathogens indicated that pathogenicity was enhanced only when host-tissue acidification was accompanied by the suppression of H2O2. Additionally, pathogenicity of both P. digitatum and P. expansum on citrus fruit was significantly enhanced by the H2O2-scavenging enzyme catalase. Based on our study and previous reports regarding the potential involvement of citric acid and catalase in green mold pathogenesis, we suggest that these compounds are strongly associated with the virulence of P. digitatum.