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Podosphaera xanthii is the main causal agent of powdery mildew (PM) on Cucurbitaceae. In Cucumis melo , the Pm - w resistance gene, which confers resistance to P . xanthii, is located on chromosome 5 in a cluster of nucleotide-binding leucine-rich repeat receptors (NLRs). We used positional cloning and transgenesis, to isolate the Pm-w WMR 29 gene encoding a coiled-coil NLR (CC-NLR). Pm-w WMR 29 conferred high level of resistance to race 1 of PM and intermediate level of resistance to race 3 of PM. Pm-w WMR 29 turned out to be a homolog of the Aphis gossypii resistance gene Vat-1 PI 161375 . We confirmed that Pm-w WMR 29 did not confer resistance to aphids, while Vat-1 PI 161375 did not confer resistance to PM . We showed that both homologs were included in a highly diversified cluster of NLRs, the Vat cluster. Specific Vat-1 PI 161375 and Pm-w WMR 29 markers were present in 10% to 13% of 678 accessions representative of wild and cultivated melon types worldwide. Phylogenic reconstruction of 34 protein homologs of Vat-1 PI 161375 and Pm-w WMR 29 identified in 24 melon accessions revealed an ancestor with four R65aa-a specific motif in the LRR domain, evolved towards aphid and virus resistance, while an ancestor with five R65aa evolved towards PM resistance. The complexity of the cluster comprising the Vat/Pm-w genes and its diversity in melon suggest that Vat homologs may contribute to the recognition of a broad range of yet to be identified pests and pathogens., (© The Author(s) 2024. Published by Oxford University Press on behalf of Nanjing Agricultural University.)

Cucumber vein yellowing virus (CVYV) is an emerging virus on cucurbits in the Mediterranean Basin, against which few resistance sources are available, particularly in melon. The melon accession PI 164323 displays complete resistance to isolate CVYV-Esp, and accession HSD 2458 presents a tolerance, i.e., very mild symptoms despite virus accumulation in inoculated plants. The resistance is controlled by a dominant allele Cvy - 1 1 , while the tolerance is controlled by a recessive allele cvy - 2 , independent from Cvy - 1 1 . Before introducing the resistance or tolerance in commercial cultivars through a long breeding process, it is important to estimate their specificity and durability. Upon inoculation with eight molecularly diverse CVYV isolates, the resistance was found to be isolate-specific because many CVYV isolates induced necrosis on PI 164323, whereas the tolerance presented a broader range. A resistance-breaking isolate inducing severe mosaic on PI 164323 was obtained. This isolate differed from the parental strain by a single amino acid change in the VPg coding region. An infectious CVYV cDNA clone was obtained, and the effect of the mutation in the VPg cistron on resistance to PI 164323 was confirmed by reverse genetics. This represents the first determinant for resistance-breaking in an ipomovirus. Our results indicate that the use of the Cvy - 1 1 allele alone will not provide durable resistance to CVYV and that, if used in the field, it should be combined with other control methods such as cultural practices and pyramiding of resistance genes to achieve long-lasting resistance against CVYV.

Thirty-one melon accessions were screened for resistance to the begomoviruses Melon chlorotic mosaic virus (MeCMV) and Tomato leaf curl New Delhi virus (ToLCNDV). Five accessions presented nearly complete resistance to both viruses. Accession IC-274014, showing the highest level of resistance to both viruses, was crossed with the susceptible cultivar Védrantais. The F 1 , F 2 , F 3 /F 4 , and both backcross progenies were mechanically inoculated with MeCMV. Plants without symptoms or virus detection by enzyme-linked immunosorbent assay and/or PCR were considered as resistant. The segregations were compatible with two recessive and one dominant independent genes simultaneously required for resistance. Inheritance of resistance to ToLCNDV in the F 2 was best explained by one recessive gene and two independent dominant genes simultaneously required. Some F 3 and F 4 families selected for resistance to MeCMV also were resistant to ToLCNDV, suggesting that common or tightly linked genes were involved in resistance to both viruses. We propose the names begomovirus resistance-1 and Begomovirus resistance-2 for these genes (symbols bgm-1 and Bgm-2 ). Resistance to MeCMV in IC-274014 was controlled by bgm-1 , Bgm-2 , and the recessive gene melon chlorotic mosaic virus resistance ( mecmv ); resistance to ToLCNDV was controlled by bgm-1 , Bgm-2 , and the dominant gene Tomato leaf curl New Delhi virus resistance ( Tolcndv ).

Background: A number of molecular marker linkage maps have been developed for melon (Cucumis melo L.) over the last two decades. However, these maps were constructed using different marker sets, thus, making comparative analysis among maps difficult. In order to solve this problem, a consensus genetic map in melon was constructed using primarily highly transferable anchor markers that have broad potential use for mapping, synteny, and comparative quantitative trait loci (QTL) analysis, increasing breeding effectiveness and efficiency via marker-assisted selection (MAS)., Results: Under the framework of the International Cucurbit Genomics Initiative (ICuGI, http://www.icugi.org), an integrated genetic map has been constructed by merging data from eight independent mapping experiments using a genetically diverse array of parental lines. The consensus map spans 1150 cM across the 12 melon linkage groups and is composed of 1592 markers (640 SSRs, 330 SNPs, 252 AFLPs, 239 RFLPs, 89 RAPDs, 15 IMAs, 16 indels and 11 morphological traits) with a mean marker density of 0.72 cM/marker. One hundred and ninety-six of these markers (157 SSRs, 32 SNPs, 6 indels and 1 RAPD) were newly developed, mapped or provided by industry representatives as released markers, including 27 SNPs and 5 indels from genes involved in the organic acid metabolism and transport, and 58 EST-SSRs. Additionally, 85 of 822 SSR markers contributed by Syngenta Seeds were included in the integrated map. In addition, 370 QTL controlling 62 traits from 18 previously reported mapping experiments using genetically diverse parental genotypes were also integrated into the consensus map. Some QTL associated with economically important traits detected in separate studies mapped to similar genomic positions. For example, independently identified QTL controlling fruit shape were mapped on similar genomic positions, suggesting that such QTL are possibly responsible for the phenotypic variability observed for this trait in a broad array of melon germplasm., Conclusions: Even though relatively unsaturated genetic maps in a diverse set of melon market types have been published, the integrated saturated map presented herein should be considered the initial reference map for melon. Most of the mapped markers contained in the reference map are polymorphic in diverse collection of germplasm, and thus are potentially transferrable to a broad array of genetic experimentation (e.g., integration of physical and genetic maps, colinearity analysis, map-based gene cloning, epistasis dissection, and marker-assisted selection).

Sex determination in plants leads to the development of unisexual flowers from an originally bisexual floral meristem. This mechanism results in the enhancement of outcrossing and promotes genetic variability, the consequences of which are advantageous to the evolution of a species. In melon, sexual forms are controlled by identity of the alleles at the andromonoecious (a) and gynoecious (g) loci. We previously showed that the a gene encodes an ethylene biosynthesis enzyme, CmACS-7, that represses stamen development in female flowers. Here we show that the transition from male to female flowers in gynoecious lines results from epigenetic changes in the promoter of a transcription factor, CmWIP1. This natural and heritable epigenetic change resulted from the insertion of a transposon, which is required for initiation and maintenance of the spreading of DNA methylation to the CmWIP1 promoter. Expression of CmWIP1 leads to carpel abortion, resulting in the development of unisexual male flowers. Moreover, we show that CmWIP1 indirectly represses the expression of the andromonoecious gene, CmACS-7, to allow stamen development. Together our data indicate a model in which CmACS-7 and CmWIP1 interact to control the development of male, female and hermaphrodite flowers in melon.

Andromonoecy is a widespread sexual system in angiosperms characterized by plants carrying both male and bisexual flowers. In melon, this sexual form is controlled by the identity of the alleles at the andromonoecious (a) locus. Cloning of the a gene reveals that andromonoecy results from a mutation in the active site of 1-aminocyclopropane-1-carboxylic acid synthase. Expression of the active enzyme inhibits the development of the male organs and is not required for carpel development. A causal single-nucleotide polymorphism associated with andromonoecy was identified, which suggests that the a allele has been under recent positive selection and may be linked to the evolution of this sexual system.

The characterization of natural recessive resistance genes and virus-resistant mutants of Arabidopsis have implicated translation initiation factors of the 4E family [eIF4E and eIF(iso)4E] as susceptibility factors required for virus multiplication and resistance expression. To date, viruses controlled by these genes mainly belong to the family Potyviridae. Melon necrotic spot virus (MNSV) belongs to the family Tombusviridae (genus Carmovirus) and is an uncapped and non-polyadenylated RNA virus. In melon, nsv-mediated resistance is a natural source of recessive resistance against all strains of MNSV except MNSV-264. Analyses of chimeras between non-resistance-breaking and resistance-breaking strains have shown that the avirulence determinant maps to the 3'-untranslated region (3'-UTR) of the viral genome. Using a combination of positional cloning and microsynteny analysis between Arabidopsis thaliana and melon, we genetically and physically delimited the nsv locus to a single bacterial artificial chromosome clone and identified the melon eukaryotic translation initiation factor 4E (Cm-eIF4E) as a candidate gene. Complementation analysis using a biolistic transient expression assay, confirmed Cm-eIF4E as the product of nsv. A single amino acid change at position 228 of the protein led to the resistance to MNSV. Protein expression and cap-binding analysis showed that Cm-eIF4E encoded by a resistant plant was not affected in it's cap-binding activity. The Agrobacterium-mediated transient expression of the susceptibility allele of Cm-eIF4E in Nicotiana benthamiana enhanced MNSV-264 accumulation. Based on these results, a model to explain melon resistance to MNSV is proposed. These data, and data from other authors, suggest that translation initiation factors of the eIF4E family are universal determinants of plant susceptibility to RNA viruses.

Background: The genus Cucurbita (pumpkin, squash, gourd) is native to the Americas and diffused to other continents subsequent to the European contact in 1492. For many years, the earliest images of this genus in Europe that were known to cucurbit specialists were the two illustrations of C. pepo pumpkins that were published in Fuchs' De Historia Stirpium, 1542. Images of fruits of two Cucurbita species, drawn between 1515 and 1518, were recently discovered in the Villa Farnesina in Rome., Findings: An even earlier image of Cucurbita exists in the prayer book, Grandes Heures d'Anne de Bretagne, illustrated by Jean Bourdichon in Touraine, France, between 1503 and 1508. This image, which shows a living branch bearing flowers and fruits, had not been examined and analysed by cucurbit specialists until now. The image is identified as depicting Cucurbita pepo subsp. texana. Unlike some of the fruits of Cucurbita depicted in the Villa Farnesina a decade later, this image does not depict an esculent and does not constitute evidence of early European contact with New World agriculture. Based on the descriptive, ecological and geographical accounts of C. pepo subsp. texana in the wild, the idea is considered that the image was based on an offspring of a plant found growing along the Gulf Coast of what is now the United States.

ABSTRACT Partial resistance to downy mildew (Pseudoperonospora cubensis) and complete resistance to powdery mildew (Podosphaera xanthii races 1, 2, 3, and 5 and Golovinomyces cichoracearum race 1) were studied using a recombinant inbred line population between 'PI 124112' (resistant to both diseases) and 'Védrantais' (susceptible line). A genetic map of melon was constructed to tag these resistances with DNA markers. Natural and artificial inoculations of Pseudoperonospora cubensis were performed and replicated in several locations. One major quantitative trait loci (QTL), pcXII.1, was consistently detected among the locations and explained between 12 to 38% of the phenotypic variation for Pseudoperonospora cubensis resistance. Eight other Pseudoperonospora cubensis resistance QTL were identified. Artificial inoculations were performed with several strains of four races of Podosphaera xanthii and one race of G. cichoracearum. Two independent major genes, PmV.1 and PmXII.1, were identified and shown to be involved in the simple resistance to powdery mildew. Three digenic epistatic interactions involving four loci were detected for two races of Podosphaera xanthii and one race of G. cichoracearum. Co-localization between PmV.1, resistance genes, and resistance genes homologues was observed. Linkage between the major resistance QTL to Pseudoperonospora cubensis, pcXII.1, and one of the two resistance genes to powdery mildew, PmXII.1, was demonstrated.

ABSTRACT Fusarium oxysporum f. sp. melonis is responsible for Fusarium wilt of melon. Race 1.2 strains overcome two dominant resistance genes (Fom-1 and Fom-2) and are further divided into two types depending on the symptoms they cause, yellowing or wilting. Partial resistance to F. oxysporum f. sp. melonis race 1.2 was studied by using a recombinant inbred line (RIL) population that was developed by single seed descent from an F(1) hybrid between 'Isabelle', a partially resistant line, and a susceptible line, 'Védrantais'. Artificial inoculations were performed with a yellowing strain (TST) and a wilting strain (D'Oléon 8) and replicated in six locations. Disease reactions of the parental lines, controls, and RILs were scored using a 1-to-5 scale and by using the area under the disease progress curve (AUDPC). Phenotypic correlations were highly significant between the different locations and experiments. The heritability of the resistance was high, from 0.72 to 0.96, and 4 to 14 genetic factors were estimated to confer resistance to F. oxysporum f. sp. melonis race 1.2. Thirteen other strains were tested with an RILs subset. Some small strainspecific effects may be involved. These results contribute to a better understanding of the polygenic inheritance of the partial resistance to F. oxysporum f. sp. melonis race 1.2.

A new linkage map of Cucumis melo, derived from the F2 progeny of a cross between PI 414723 and C. melo 'TopMark' is presented. The map spans a total of 1421 cM and includes 179 points consisting of random amplified polymorphic DNA (RAPD), amplified fragment length polymorphism (AFLP), inter-simple sequence repeats (ISSRs), simple sequence repeats (SSRs), and restriction fragment length polymorphism (RFLP) markers. The map also includes an aphid resistance trait (Vat) and the sex type gene, andromonoecious (a), the two of which are important in resistance breeding and the control of hybrid seed production, as well as a seed-color gene, Wt-2. Most RFLPs represent sequence-characterized cDNA probes from C. melo and Cucumis sativus. These include resistance gene homologues and genes involved in various aspects of plant development and metabolism. A sub-set of our SSR and RFLP markers were also mapped, as part of this study, on additional mapping populations that were published for this species. This provides important reference points ("anchors"), enabling us to identify several linkage groups with respect to other melon maps.

Fruit ripening and abscission are associated with an ethylene burst in several melon (Cucumis melo) genotypes. In cantaloupe as in other climacteric fruit, exogenous ethylene can prematurely induce abscission, ethylene production, and ripening. Melon genotypes without fruit abscission or without ethylene burst also exist and are, therefore, non-climacteric. In the nonabscising melon fruit PI 161375, exogenous ethylene failed to stimulate abscission, loss of firmness, ethylene production, and expression of all target genes tested. However, the PI 161375 etiolated seedlings displayed the usual ethylene-induced triple response. Genetic analysis on a population of recombinant cantaloupe Charentais x PI 161375 inbred lines in segregation for fruit abscission and ethylene production indicated that both characters are controlled by two independent loci, abscission layer (Al)-3 and Al-4. The non-climacteric phenotype in fruit tissues is attributable to ethylene insensitivity conferred by the recessive allelic forms from PI 161375. Five candidate genes (two ACO, two ACS, and ERS) that were localized on the melon genetic map did not exhibit colocalization with Al-3 or Al-4.

Thirty-four polymorphic simple-sequence repeats (SSRs) were evaluated for length polymorphism in melon (Cucumis melo L.) and cucumber (Cucumis sativus L.). SSR markers were located on three melon maps (18 on the map of 'Vedrantais' and PI 161375, 23 on the map of 'Piel de Sapo' and PI 161375, and 16 on the map of PI 414723 and 'Dulce'). In addition, 14 of the markers were located on the cucumber map of GY14 and PI 183967. SSRs proved to be randomly distributed throughout the melon and cucumber genomes. Mapping of the SSRs in the different maps led to the cross-identification of seven linkage groups in all melon maps. In addition, nine SSRs were common to both melon and cucumber maps. The potential of SSR markers as anchor points for melon-map merging and for comparative mapping with cucumber was demonstrated.

ABSTRACT In 1993, a bacterial blight caused important losses of cantaloupe (Cucumis melo var. cantalupensis) in southwestern France and has now been reported in all cantaloupe-growing regions of France. The causal agent of this blight is Pseudomonas syringae, although on a worldwide basis this bacterium has not been a major pathogen of melon for over 50 years. To identify the pathovar of the cantaloupe pathogen, we employed biochemical tests, plasmid and chromosomal profiling, and host range studies for 23 strains from cantaloupe and 47 reference strains of 14 pathovars of P. syringae. Numerical analysis of 119 traits, serological typing, syringomycin production, and BOX-polymerase chain reaction profiles did not allow us to differentiate among pathovars related to P. syringae pv. syringae. Host range studies of cantaloupe and references strains on 18 plant species showed that virulence to sugar beet was a common feature of strains virulent on cantaloupe, but was not common to strains avirulent on cantaloupe. Virulence to other species of plants varied among strains, but the overall extent of the host range was proportional to aggressiveness to cantaloupe. We propose that the strains attacking cantaloupe in France be considered P. syringae pv. aptata and that adequate host range testing may reveal that this pathovar is the cause of cantaloupe blight reported in other parts of the world.

Melon rugose mosaic virus (MRMV) was isolated from snake cucumber (Cucumis melo var. flexuosus) in the Kassala region of Sudan in 1993. The host range of the virus was mostly limited to cucurbits, where it induced severe mosaic and leaf deformations. Cytopathological studies revealed severe chloroplast alterations, including vesicles at their periphery and the tendency to aggregate, which are typical of tymovirus infections, providing further evidence that MRMV is a tentative member of the genus Tymovirus. In melon and snake cucumber, MRMV was found to be seed transmitted at rates of 0.9 and 3.8%, respectively. Seed dissection experiments revealed that the virus could be detected in the seed coat, papery layer, and embryo. Seed disinfection treatments did not reduce seed transmission rates, which suggests an internal transmission. A preliminary screening for resistance in melon revealed some resistance in two out of 367 accessions tested.