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Comparative Proteome Analysis of the Strawberry-Fusarium oxysporum f. sp. fragariae Pathosystem Reveals Early Activation of Defense Responses as a Crucial Determinant of Host Resistance

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Figshare2016-02-19 更新2026-04-29 收录
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https://figshare.com/articles/dataset/Comparative_Proteome_Analysis_of_the_Strawberry_i_Fusarium_oxysporum_i_f_sp_i_fragariae_i_Pathosystem_Reveals_Early_Activation_of_Defense_Responses_as_a_Crucial_Determinant_of_Host_Resistance/2427811
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Fusarium wilt on strawberry caused by Fusarium oxysporum f. sp. fragariae (Fof) is a serious threat to commercial strawberry production worldwide. However, resistance mechanisms of strawberry against Fof remain unknown. To reveal the defense responses of strawberry against Fof, comparative proteome analyses were conducted to determine temporal changes in root proteomes of the resistant cv. Festival and susceptible cv. Camarosa from 4 to 72 h post inoculation with Fof. Analysis of proteins separated by two-dimensional gel electrophoresis revealed 79 Fof-responsive proteins with significant differences in abundance (P < 0.05 and greater than 2-fold) in the resistant and/or susceptible cultivar. The 79 proteins were identified through MALDI-TOF/TOF MS/MS analysis, and were mainly involved in primary, secondary and protein metabolism, stress and defense responses, antioxidant and detoxification mechanisms, and hormone biosynthesis. Among these, pathogenesis-related proteins and proteins involved in reactive oxygen species detoxification, ethylene/jasmonic acid signaling pathways, secondary metabolite biosynthesis, glycolysis and/or ubiquitin/26S proteasome-mediated protein degradation have great potential in mediating strawberry resistance against Fof. Protein modification may also have an important contribution. This study provides the first insights into strawberry resistance mechanisms against Fof, opening novel avenues to engineer new strawberry cultivars with improved disease resistance and to develop more effective and sustainable disease management strategies.
创建时间:
2016-02-19
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