Distinct colonization patterns and cDNA-AFLP transcriptome profiles in compatible and incompatible interactions between melon and different races of Fusarium oxysporum f. sp. melonis.

Sara Sestili,Alessandra Belisario,Massimo Delledonne,Annalisa Polverari,Jamshaid Hussain,Nadia Ficcadenti,Michele Scotton,Alberto Ferrarini,Laura Luongo

doi:10.1186/1471-2164-12-122

Sara Sestili, Alessandra Belisario + Show 7 more

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https://doi.org/10.1186/1471-2164-12-122

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Abstract

BackgroundFusarium oxysporum f. sp. melonis Snyd. & Hans. (FOM) causes Fusarium wilt, the most important infectious disease of melon (Cucumis melo L.). The four known races of this pathogen can be distinguished only by infection on appropriate cultivars. No molecular tools are available that can discriminate among the races, and the molecular basis of compatibility and disease progression are poorly understood. Resistance to races 1 and 2 is controlled by a single dominant gene, whereas only partial polygenic resistance to race 1,2 has been described. We carried out a large-scale cDNA-AFLP analysis to identify host genes potentially related to resistance and susceptibility as well as fungal genes associated with the infection process. At the same time, a systematic reisolation procedure on infected stems allowed us to monitor fungal colonization in compatible and incompatible host-pathogen combinations.ResultsMelon plants (cv. Charentais Fom-2), which are susceptible to race 1,2 and resistant to race 1, were artificially infected with a race 1 strain of FOM or one of two race 1,2 w strains. Host colonization of stems was assessed at 1, 2, 4, 8, 14, 16, 18 and 21 days post inoculation (dpi), and the fungus was reisolated from infected plants. Markedly different colonization patterns were observed in compatible and incompatible host-pathogen combinations. Five time points from the symptomless early stage (2 dpi) to obvious wilting symptoms (21 dpi) were considered for cDNA-AFLP analysis. After successful sequencing of 627 transcript-derived fragments (TDFs) differentially expressed in infected plants, homology searching retrieved 305 melon transcripts, 195 FOM transcripts expressed in planta and 127 orphan TDFs. RNA samples from FOM colonies of the three strains grown in vitro were also included in the analysis to facilitate the detection of in planta-specific transcripts and to identify TDFs differentially expressed among races/strains.ConclusionOur data suggest that resistance against FOM in melon involves only limited transcriptional changes, and that wilting symptoms could derive, at least partially, from an active plant response.We discuss the pathogen-derived transcripts expressed in planta during the infection process and potentially related to virulence functions, as well as transcripts that are differentially expressed between the two FOM races grown in vitro. These transcripts provide candidate sequences that can be further tested for their ability to distinguish between races.Sequence data from this article have been deposited in GenBank, Accession Numbers: HO867279-HO867981.

Highlights

Fusarium oxysporum f. sp. melonis Snyd. & Hans. (FOM) causes Fusarium wilt, the most important infectious disease of melon (Cucumis melo L.)
Both race 1 and race 1,2 were recovered from the stems of inoculated plants, irrespective of the compatibility of the host-pathogen combination, but the strains differed in the speed and extent of colonization
In the late phase (1421 dpi), continuous distribution was observed for all three strains, but for race-specific reasons (Figure 2). Both virulent strains were continuously distributed along the entire stem length, whereas the avirulent strain was continuously absent from the highest section of the stem, and continuously present in the lower

Summary

Introduction

Fusarium oxysporum f. sp. melonis Snyd. & Hans. (FOM) causes Fusarium wilt, the most important infectious disease of melon (Cucumis melo L.). (FOM) causes Fusarium wilt, the most important infectious disease of melon (Cucumis melo L.). Pathogenic F. oxysporum strains have been subdivided into over 70 different host-specific forms (FOM) is specific to melon (Cucumis melo L.) and it is responsible for the most important infectious disease in this fruit species [4]. Race 0 induces disease on melon genotypes that lack FOM resistance genes. Independently-inherited resistance (R) genes (Fom-1 and Fom-2) provide resistance to races 0 and 2, and races 0 and 1, respectively [5]. The presence of both genes confers high resistance to races 0, 1, and 2 [6]. A major recessive QTL for resistance was located and linked to a locus controlling fruit netting [12]

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