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

Background: Fusarium 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. Results: Melon 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. Conclusion: Our 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

3D analysis of child facial dimensions for design of medical devices in low-middle income countries (LMIC).

BACKGROUND:Facial anthropometric data are scarce in African children. However, such data may be useful for the design of medical devices for high disease burden settings. The aim of this study was to obtain 3D facial anthropometric data of Congolese children aged 0-5 years. METHODS & FINDINGS:The faces of 287 Congolese children were successfully scanned using a portable structured-light based 3D video camera, suitable for field work in low- income settings. The images were analyzed using facial analysis algorithms. Normal growth curves were generated for the following facial dimensions: distance between nares and distance from subnasion to upper lip. At birth, 1 year, and 5 years of age the median dimensions were: 13·92, 14·66, and 17.60 mm, respectively for distance between nares, and 10·16, 10.88, and 13·79 mm, respectively for distance from subnasion to upper lip. Modeled facial contours conveniently clustered into three average sizes which could be used as templates for the design of medical instruments. CONCLUSION:Capturing of 3D images of infants and young children in LMICs is feasible using portable cameras and computerized analysis. This method and these specific data on Congolese pediatric facial dimensions may assist in the design of appropriately sized medical devices (thermometers, face masks, pulse oximeters, etc.) for this population

Dual Resistance of Melon to Fusarium oxysporum Races 0 and 2 and to Papaya ring-spot virus is Controlled by a Pair of Head-to-Head-Oriented NB-LRR Genes of Unusual Architecture

International audiencePotyviruses such as Papaya ring-spot virus (PRSV) cause important yield losses in cucurbits. Two distinct resistant alleles were identified in the Cucumis melo germplasm. Accession PI 414723 ( Supplemental Table 1) possesses mono-genic resistance, controlled by the Prv2 allele, and reacts to PRSV by systemic necrotic lesions; plants with the Prv1 allele, described in cultivar WMR-29, remain symptomless (Pitratand Lecoq, 1983). Fusarium oxysporum f. sp. melonis (FUS) exclusively attacks melon, causing severe wilt. Monogenic dominant resistance was described against races 0, 1, and 2. The Fom-2 gene, controlling resistance to races 0 and 1, was cloned by Joobeur et al. (2004), and encodes a nucleotide binding domain (NB)–leucine rich repeat (LRR) protein. Our study focused on the Fom-1 gene, which confers resistance to races 0 and 2 (Risser et al., 1976), and on the Prv gene; the two are tightly linked on melon linkage group IX. Molecular markers were developed for the Fom-1/Prv locus, but no study has provided the resolution required for positional cloning

Dual Resistance of Melon to Fusarium oxysporum Races 0 and 2 and to Papaya ring-spot virus is Controlled by a Pair of Head-to-Head-Oriented NB-LRR Genes of Unusual Architecture

International audiencePotyviruses such as Papaya ring-spot virus (PRSV) cause important yield losses in cucurbits. Two distinct resistant alleles were identified in the Cucumis melo germplasm. Accession PI 414723 ( Supplemental Table 1) possesses mono-genic resistance, controlled by the Prv2 allele, and reacts to PRSV by systemic necrotic lesions; plants with the Prv1 allele, described in cultivar WMR-29, remain symptomless (Pitratand Lecoq, 1983). Fusarium oxysporum f. sp. melonis (FUS) exclusively attacks melon, causing severe wilt. Monogenic dominant resistance was described against races 0, 1, and 2. The Fom-2 gene, controlling resistance to races 0 and 1, was cloned by Joobeur et al. (2004), and encodes a nucleotide binding domain (NB)–leucine rich repeat (LRR) protein. Our study focused on the Fom-1 gene, which confers resistance to races 0 and 2 (Risser et al., 1976), and on the Prv gene; the two are tightly linked on melon linkage group IX. Molecular markers were developed for the Fom-1/Prv locus, but no study has provided the resolution required for positional cloning