Abstract

Little is known about the histologic features of a latent Monilinia fructicola infection and brown rot in infected fruit. This report informs on the results of an investigation whose aim was to analyze the microanatomy of nectarines with a latent and visible M. fructicola infection. Mature nectarines were inoculated with an M. fructicola isolate and incubated at 25°C for 0, 24, 48, 72, or 96 hours in the dark. For investigating the latent infection process, the inoculated nectarines were first incubated at 25°C for 24 hours in the dark and then incubated at 4°C for 72, 144, 216, and 288 hours in the dark. At the end of the incubation, samples of nectarine tissue were excised from the inoculation points and prepared for light and transmission electron microscopic examinations. No signs of disease were seen on the surface of nectarines with a latent infection over the 288-hour incubation period. When the tissue samples were microscopically examined, M. fructicola colonized the stomata and this stomatal colonization progressively increased over time and was associated with gradual collapse of the epidermal cells and colonization of the subepidermis. In nectarines with visible brown rot, the disease usually appeared after 24 hours on the surface and in the uppermost layers of epidermal cells, which began to collapse after 48 hours. Subsequently, the diseased tissues of the nectarines displayed (a) colonization of the epidermis and mesocarp by M. fructicola with thin and thick hyphae, (b) collapse and disruption of epidermal and mesocarpic cells, (c) lysogenic cavities in the subepidermis and mesocarp, (d) degradation of the cuticle and epidermis, and (e) M. fructicola sporulation. M. fructicola is active during latent infections because slow and progressive colonization of nectarine subcuticular cells by the fungus occurs.

Highlights

  • Brown rot is an economically important fungal disease of peaches (Prunus persica (L.) Batch) and nectarines (P. persica var. nectarina (Aiton) Maxim), and is responsible for substantial pre-harvest and post-harvest losses [1]

  • The intercellular hyphae, which had invaded mesocarpic cells, were ultrastructurally different from the intracellular hyphae: their cytoplasm contained no vesicles and their cell walls were thick (Fig 4D and 4E). The aim of this investigation was to analyze the microanatomy of nectarines with a latent and a visible M. fructicola infection using light microscopy and Transmission electron microscopic (TEM)

  • Tissues of mature nectarines with latent M. fructicola infections are characterized by the presence of intercellular hyphae at the subcuticular level

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Summary

Introduction

Brown rot is an economically important fungal disease of peaches (Prunus persica (L.) Batch) and nectarines (P. persica var. nectarina (Aiton) Maxim), and is responsible for substantial pre-harvest and post-harvest losses [1]. Brown rot is an economically important fungal disease of peaches (Prunus persica (L.) Batch) and nectarines In Spain, brown rot is caused by three Monilinia spp.: M. fructicola (G Winter) Honey, M. fructigena (Aderhold & Ruhland) Honey, and M. laxa (Aderhold & Ruhland) Honey [2], and of these three fungi, M. fructicola has the fastest growth rate and is the most aggressive one [3]. Fruit can be infected with Monilinia spp. at PLOS ONE | DOI:10.1371/journal.pone.0160675. Microanatomy of Brown Rot Infection any stage of its development, disease incidence increases and the index of disease severity becomes greater with fruit ripening [4,5,6]. Brown rot on ripening or mature fruit typically develops as a rapidly spreading, firm, brown decay. The decay of ripe infected peach and nectarine fruit may become visible within 48–72 hours of infection [2]

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