کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4367096 | 1616621 | 2013 | 10 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Genetic structure and natural variation associated with host of origin in Penicillium expansum strains causing blue mould Genetic structure and natural variation associated with host of origin in Penicillium expansum strains causing blue mould](/preview/png/4367096.png)
• Host influence on patulin as P. expansum pathogenicity/virulence factor was investigated.
• Three P. expansum strain groups were grown on their hosts of isolation and derived media.
• For each group, the highest aggressiveness and toxigenicity were recorded on the host of isolation.
• Host effect on toxin production appeared to be exerted at a transcriptional level.
• A HRM method herein set up permitted to group strains according to the host of origin.
Blue mould, caused by Penicillium expansum, is one of the most economically damaging postharvest diseases of pome fruits, although it may affect a wider host range, including sweet cherries and table grapes. Several reports on the role of mycotoxins in plant pathogenesis have been published, but few focussed on the influence of mycotoxins on the variation in host preference amongst producing fungi. In the present study the influence of the host on P. expansum pathogenicity/virulence was investigated, focussing mainly on the relationship with patulin production. Three P. expansum strain groups, originating from apples, sweet cherries, and table grapes (7 strains per host) were grown on their hosts of isolation and on artificial media derived from them. Strains within each P. expansum group proved to be more aggressive and produced more patulin than the other two groups under evaluation when grown on the host from which they originated. Table grape strains were the most aggressive (81% disease incidence) and strongest patulin producers (up to 554 μg/g). The difference in aggressiveness amongst strains was appreciable only in the presence of a living host, suggesting that the complex pathogen–host interaction significantly influenced the ability of P. expansum to cause the disease. Incidence/severity of the disease and patulin production proved to be positively correlated, supporting the role of patulin as virulence/pathogenicity factor. The existence of genetic variation amongst isolates was confirmed by the High Resolution Melting method that was set up herein, which permitted discrimination of P. expansum from other species (P. chrysogenum and P. crustosum) and, within the same species, amongst the host of origin. Host effect on toxin production appeared to be exerted at a transcriptional level.
Journal: International Journal of Food Microbiology - Volume 165, Issue 2, 15 July 2013, Pages 111–120