Project description:Viruses are among the most destructive and difficult to control plant pathogens. Melon (Cucumismelo L.) has become the model species for the agriculturally important Cucurbitaceae family. Approaches that take advantage of recently developed genomic tools in melon are being extremely useful for understanding viral pathogenesis and can contribute to the identification of target genes to breed new resistant cultivars. In this work, we have used a recently described melon microarray for transcriptome profiling of two melon cultivars infected with two strains of Melon necrotic spot virus (MNSV) that only differ on their 3´-untranslated regions. Tissues of melon plants from cultivars Out of 7566 and 7074 genes deregulated by MNSV-Mα5 and MNSV-Mα5/3’264, 1851 and 1356, respectively, were strain-specific. Likewise, MNSV-Mα5/3’264 specifically deregulated 2925 and 1618 genes in Planters Jumbo and Tendral, respectively. Thus, significantly affected GO categories were clearly different for the different virus/host combinations. Grouping genes according to their patterns of expression allowed the identification of two groups specifically deregulated by MNSV-Mα5/3’264 with respect to MNSV-Mα5 in Tendral, and one group antagonistically regulated in Planters Jumbo vs. Tendral after MNSV-Mα5/3’264 infection. Genes in these three groups belong to a diversity of functional classes, and no obvious regulatory commonalities were identified. When data on MNSV-Mα5/Tendral infections were compared to equivalent data on cucumber mosaic virus or watermelon mosaic virus infections, cytokinin-O-glucosyltransferase2 was identified as the only gene deregulated by the three viruses, with infections dynamics correlating with the amplitude of transcriptome remodeling. Both common and strain-specific changes, as well as common but also cultivar-specific changes, have been identified by profiling transcriptomes of plants from two melon cultivars infected with two MNSV strains. No obvious regulatory features shared among deregulated genes have been identified, pointing toward regulation through differential functional implications. Viruses are among the most destructive and difficult to control plant pathogens. Melon (Cucumismelo L.) has become the model species for the agriculturally important Cucurbitaceae family. Approaches that take advantage of recently developed genomic tools in melon are being extremely useful for understanding viral pathogenesis and can contribute to the identification of target genes to breed new resistant cultivars. In this work, we have used a recently described melon microarray for transcriptome profiling of two melon cultivars infected with two strains of Melon necrotic spot virus (MNSV) that only differ on their 3´-untranslated regions. Tissues of melon plants from cultivars Out of 7566 and 7074 genes deregulated by MNSV-Mα5 and MNSV-Mα5/3’264, 1851 and 1356, respectively, were strain-specific. Likewise, MNSV-Mα5/3’264 specifically deregulated 2925 and 1618 genes in Planters Jumbo and Tendral, respectively. Thus, significantly affected GO categories were clearly different for the different virus/host combinations. Grouping genes according to their patterns of expression allowed the identification of two groups specifically deregulated by MNSV-Mα5/3’264 with respect to MNSV-Mα5 in Tendral, and one group antagonistically regulated in Planters Jumbo vs. Tendral after MNSV-Mα5/3’264 infection. Genes in these three groups belong to a diversity of functional classes, and no obvious regulatory commonalities were identified. When data on MNSV-Mα5/Tendral infections were compared to equivalent data on cucumber mosaic virus or watermelon mosaic virus infections, cytokinin-O-glucosyltransferase2 was identified as the only gene deregulated by the three viruses, with infections dynamics correlating with the amplitude of transcriptome remodeling. Both common and strain-specific changes, as well as common but also cultivar-specific changes, have been identified by profiling transcriptomes of plants from two melon cultivars infected with two MNSV strains. No obvious regulatory features shared among deregulated genes have been identified, pointing toward regulation through differential functional implications.

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