الفهرس | Only 14 pages are availabe for public view |
Abstract In this study, it was possible to inhibit B. cinerea fungal growth severity in harvested rip strawberry fruits through the proactive priming of fruits resistance by UV-B light (290-315 nm). We irradiated harvested fruits with different UV-B light amounts (0, 0.33, 0.65, and 1.3 mJoule/cm2 ) before artificially infecting them with B. cinerea. The molecular confirmation using B. cinerea specific Cutinase A gene estimated a reduction ratio of 50% in fungal DNA with fruits proactively exposed to UV-B (1.3 mJoule/cm2 ) compared to non-UV-B (0 mJoule/cm2 ) treated fruits which were totally rotted with velvety gray mold growth. To reveal possible molecular mechanism behind UV-B induced resistance against B. cinerea, the expression profiles of several resistance-relatedgenes were quantified using real-time PCR assay in the fruits on day 1 and day 2after infection. UV-B light significantly peaked up the expression of the pathogenesis-related (PR) gene FaBG2-1, which encodes the fungal cell wall degrading enzyme β-1-3-glucanase. Furthermore, the jasmonic acid (JA) biosynthesis key gene FaAOS was dramatically induced after exposure to UV-Bwith infected or non-infected fruits on day 2 in particular. Interestingly, volatile terpenoids linalool/nerolidol synthase gene (FaNES1) expression was also elevated in response to UV-B treatment. ABA signaling gene FaPYR1 was also found to be responsive after 2 days. Collectively, it is suggested that UV-B proactive treatment could urge strawberry ripe fruits biological defenses prior anypossible fungal infection. Thus UV-B irradiation could be considered as a sustainable method for controlling fungal infection in ripe strawberry fruits postharvest |