Abstract:
Very few studies have investigated the host-pathogen interaction of Penicillium spp. on nectarine. Penicillium digitatum was identified as pathogenic and highly aggressive on nectarine. A strong association was made with host age/ripeness. This points to a new mechanism or life strategy used by P. digitatum to infect and colonize previously thought nonhosts. The aim of this study was to determine the effect of postharvest storage of nectarine on the infection and colonization of P. digitatum and Penicillium expansum at molecular and physical (firmness and pH) levels. The impact of environmental conditions (cold storage) and pathogen pressure (inoculum load) was also investigated. Although disease incidence was much lower, lesions caused by P. digitatum were similar in size to those caused by P. expansum on freshly harvested nectarine. Disease incidence and lesion diameter significantly increased (larger than P. expansum) on longer stored fruit. Cold storage had the largest effect on P. digitatum. Inoculum load had a meaningful effect on both Penicillium spp. Storage significantly affected pH modulation and gene expression. The pathogens not only decreased but also, increased and maintained (similar to initial pH of the host) pH of infected tissue. The polygalacturonase (PG) gene and creA were upregulated by P. digitatum on 7-day postharvest fruit (other genes were unaffected). It partly explains the larger lesions on older or riper fruit. A different expression profile was observed from P. expansum: strong downregulation in PG and slight upregulation in pacC. Very different life strategies were used by the two Penicillium spp. when infecting nectarine. Unlike what is known on citrus, P. digitatum showed an opportunistic lifestyle that takes advantage of specific host and environmental conditions. It is largely still unclear (gene expression) what specifically triggers the increase in disease incidence (infection) and lesion diameter (colonization) of P. digitatum on older or riper fruit. The differences between in vivo and in vitro studies make it difficult to directly correlate results. Additional research is still needed to differentiate and understand the infection and colonization of these pathogens on the same host.
