Characterization of the watermelon seedling infection process by Fusarium oxysporum f. sp niveum

文献类型： 外文期刊

第一作者： Zhang, M.

作者： Zhang, M.;Xu, J. H.;Liu, G.;Yao, X. F.;Li, P. F.;Yang, X. P.

作者机构：

关键词： anatomy;Citrullus lanatus;defence gene expression;Fusarium oxysporum f. sp niveum;green fluorescent protein

期刊名称：PLANT PATHOLOGY （ 影响因子：2.59； 五年影响因子：2.924 ）

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收录情况： SCI

摘要： Fusarium oxysporum f. sp. niveum (FON) is the causal pathogen of fusarium wilt in watermelon. Understanding the interactions of watermelon seedlings and FON is of scientific and practical importance for disease control. The colonization dynamics of a susceptible watermelon cultivar, Sumi 1 (SM 1), were visualized using a green fluorescent protein (GFP)-expressing strain of FON race 1 (FON 1-GFP). Within 2 days post-inoculation (dpi), hyphae adhered to and grew on epidermal cells. At 3 dpi, hyphae crossed the epidermis, penetrated into the cortex and progressed through parenchymal cell borders reaching the xylem vessels at 7 dpi. Growth of hyphae was restricted to the xylem vessels even in the colonized lower hypocotyl. The responses of SM 1 seedlings to infection were analysed. In the roots of SM 1, infected xylem vessels were plugged with gums and tyloses and some occluded vessels were shed from the root vascular tissue. Parenchyma cells surrounding the vascular cylinder showed wall thickening and cell disintegration, which eventually formed cavities. Hypocotyls of most SM 1 plants were also infected. Vascular tissues were densely colonized by hyphae until the vascular bundle became hollow and plants withered. Moreover, the expression patterns of six defence-related genes in roots of SM 1 were analysed using real-time quantitative PCR. Transcript levels of plant defensin-like genes ClPDF2.1 and ClPDF2.4, phenylalanine ammonia lyase (PAL), chitinase (CHI) and ascorbate peroxidase (APX) were significantly induced in SM 1 roots during FON 1 infection, while polyphenoloxidase (PPO) did not show significant responses to FON 1 infection.

分类号： S432.1

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