QTL Mapping for Gummy Stem Blight Resistance in Watermelon (Citrullus spp.).
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SUBMITTER: Lee ES
PROVIDER: S-EPMC7999335 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Key messageWe identified QTLs associated with gummy stem blight resistance in an interspecific F2:3 Citrullus population and developed marker assays for selection of the loci in watermelon. Gummy stem blight (GSB), caused by three Stagonosporopsis spp., is a devastating fungal disease of watermelon (Citrullus lanatus) and other cucurbits that can lead to severe yield losses. Currently, no commercial cultivars with genetic resistance to GSB in the field have been reported. Utilizing GSB-resistant cultivars would reduce yield losses, decrease the high cost of disease control, and diminish hazards resulting from frequent fungicide application. The objective of this study was to identify quantitative trait loci (QTLs) associated with GSB resistance in an F2:3 interspecific Citrullus mapping population (N = 178), derived from a cross between Crimson Sweet (C. lanatus) and GSB-resistant PI 482276 (C. amarus). The population was phenotyped by inoculating seedlings with Stagonosporopsis citrulli 12178A in the greenhouse in two separate experiments, each with three replications. We identified three QTLs (ClGSB3.1, ClGSB5.1 and ClGSB7.1) associated with GSB resistance, explaining between 6.4 and 21.1% of the phenotypic variation. The genes underlying ClGSB5.1 includes an NBS-LRR gene (ClCG05G019540) previously identified as a candidate gene for GSB resistance in watermelon. Locus ClGSB7.1 accounted for the highest phenotypic variation and harbors twenty-two candidate genes associated with disease resistance. Among them is ClCG07G013230, encoding an Avr9/Cf-9 rapidly elicited disease resistance protein, which contains a non-synonymous point mutation in the DUF761 domain that was significantly associated with GSB resistance. High throughput markers were developed for selection of ClGSB5.1 and ClGSB7.1. Our findings will facilitate the use of molecular markers for efficient introgression of the resistance loci and development of GSB-resistant watermelon cultivars.
| S-EPMC7843542 | biostudies-literature
Project description:BackgroundGummy stem blight (GSB), caused by Didymella bryoniae (syn. Stagonosporopsis cucurbitacearum), produces devastating symptoms on whole plants of watermelon (Citrullus lanatus) and other cucurbits, significantly reducing yield and quality. Identification of genetic determinants and sources of resistance to this devastating GSB disease in watermelon is essential for developing resistant varieties.ResultsIn this study, we aimed at identifying quantitative trait loci (QTLs) linked to GSB resistance in melon. We identified the genome-wide single nucleotide polymorphisms (SNPs) by genotyping by sequencing (GBS) of an F2 population developed from C. lanatus lines, 'PI 279461' (resistant) ✕ 'PI 223764' (susceptible). Inheritance analysis indicated that resistance to GSB is a multi-genic trait in this population. Three QTLs namely, ClGSB1.1, ClGSB10.1, and ClGSB11.1 associated with GSB resistance, explaining approximately 10% of the phenotypic variation, were identified. Among these, the QTL ClGSB1.1 on chromosome 1 is identified as a major QTL harboring five candidate genes associated with GSB resistance including two RLKs (ClC01G014900 and ClC01G015010), two WRKY transcription factors (ClC01G014910 and ClC01G014990), and one AvrRpt-cleavage domain protein (ClC01G015130).ConclusionTwo high resolution melting (HRM) markers, WmGSB1.1-2 and WmGSB1.1-7 having a high positive correlation with the phenotypic variations, were developed. Five potential candidate genes were predicted to be associated with GSB resistance. These findings will help breeders to develop watermelon cultivars resistant to GSB.
| S-EPMC9441027 | biostudies-literature
Project description:Watermelon (Citrullus lanatus) is a nutritionally rich and economically important horticultural crop of the Cucurbitaceae family. Gummy stem blight (GSB) is a major disease of watermelon, which is caused by the fungus Didymella bryoniae, and results in substantial economic losses in terms of yield and quality. However, only a few molecular studies have focused on GSB resistance in watermelon. Nucleotide binding site (NBS)-encoding resistance (R) genes play important roles in plant defense responses to several pathogens, but little is known about the role of NBS-encoding genes in disease resistance in watermelon. The analyzed NBS-encoding R genes comprises several domains, including Toll/interleukin-1 receptor(TIR), NBS, leucine-rich repeat (LRR), resistance to powdery mildew8(RPW8) and coiled coil (CC), which are known to be involved in disease resistance. We determined the expression patterns of these R genes in resistant and susceptible watermelon lines at different time points after D. bryoniae infection by quantitative RT-PCR. The R genes exhibited various expression patterns in the resistant watermelon compared to the susceptible watermelon. Only six R genes exhibited consistent expression patterns (Cla001821, Cla019863, Cla020705, Cla012430, Cla012433 and Cla012439), which were higher in the resistant line compared to the susceptible line. Our study provides fundamental insights into the NBS-LRR gene family in watermelon in response to D. bryoniae infection. Further functional studies of these six candidate resistance genes should help to advance breeding programs aimed at improving disease resistance in watermelons.
| S-EPMC6412240 | biostudies-literature
Project description:Gummy stem blight (GSB) causes enormous losses to melon (Cucumismelo L.) production worldwide. We aimed to develop useful molecular markers linked to GSB resistance. In this study, 168 F2 plants were obtained from the F₁ population of a cross between the GSB-susceptible 'Cornell ZPPM 339' and the GSB-resistant 'PI482399' lines. A 3:1 ratio of susceptible and resistant genotypes was observed in the F₂ population, indicating control by a single recessive gene. Nucleotide-binding site leucine-rich repeat (NBS-LRR) genes confer resistance against insects and diseases in cucurbits including melon. We cloned and sequenced the TIR-NBS-LRR-type resistance gene MELO3C022157, located on melon chromosome 9, from resistant and susceptible lines. Sequence analysis revealed deletions in the first intron, a 2-bp frameshift deletion from the second exon and a 7-bp insertion in the 4th exon of the resistant line. We developed two insertion/deletion (InDel) markers, GSB9-kh-1 and GSB9-kh-2, which were found in the first intron of MELO3C022157 linked to GSB resistance. We validated these markers with the F₂ population and inbred lines. These InDels may be used to facilitate marker-assisted selection of GSB resistance in melon. However, functional analysis of overexpressing and/or knock-down mutants is needed to confirm the frameshift mutation.
| S-EPMC6213961 | biostudies-literature
Project description:Gummy stem blight (GSB), caused by Didymella bryoniae, is one of the most devastating diseases that severely reduces cucumber production. Developing resistant varieties would be an effective strategy to control GSB. Although several GSB-resistant QTLs have been reported, causal genes for GSB resistance have not yet been identified in cucumber. A novel loci gsb3.1 for seedling GSB resistance from the "PI 183967" genotype was previously identified in a 1.7-Mb interval on chromosome 3. In this study, we developed a residual heterozygous line-derived strategy from Recombinant Inbred Lines to perform fine mapping, and with this approach, the gsb3.1 locus was narrowed to a 38 kb interval. There were six predicted genes at the gsb3.1 locus, four of which differed in expression in the GSB-resistant compared to the susceptible lines after fungal inoculation. These candidate genes (Csa3G020050, Csa3G020060, Csa3G020090, and Csa3G020590) within the gsb3.1 locus could be helpful for the genetic study of GSB resistance and marker-assisted selection in cucumber. Phylogenetic analyses indicated that the resistant gsb3.1 allele may uniquely exist in the wild species present in the Indian group, and that nucleotide diversity was significantly reduced in cultivated accessions. Therefore, the gsb3.1 allele could be introgressed into existing commercial cultivars and combined with other resistance QTLs to provide broad-spectrum and robust GSB resistance in cucumber.
| S-EPMC9480501 | biostudies-literature
Project description:Key messageFine-mapping separated Qfhs.ifa-5A into a major QTL mapping across the centromere and a minor effect QTL positioned at the distal half of 5AS. Both increase Fusarium resistance and anther extrusion. The Fusarium head blight (FHB) resistance QTL Qfhs.ifa-5A resides in the low-recombinogenic pericentromeric region of chromosome 5A making fine-mapping particularly arduous. Qfhs.ifa-5A primarily contributes resistance to fungal entry with the favorable allele descending from the highly Fusarium resistant cultivar Sumai-3. Fine-mapping a near-isogenic recombinant inbred line population partitioned the Qfhs.ifa-5A interval into 12 bins. Near-isogenic lines recombining at the interval were phenotyped for FHB severity, anther retention and plant height. Composite interval mapping separated the initially single QTL into two QTL. The major effect QTL Qfhs.ifa-5Ac mapped across the centromere and the smaller effect QTL Qfhs.ifa-5AS mapped to the distal half of 5AS. Although Qfhs.ifa-5Ac and Qfhs.ifa-5AS intervals were as small as 0.1 and 0.2 cM, their corresponding physical distances were large, comprising 44.1 Mbp and 49.2 Mbp, respectively. Sumai-3 alleles at either QTL improved FHB resistance and increased anther extrusion suggesting a pleiotropic effect of anthers on resistance. This hypothesis was supported by greenhouse experiments using the susceptible cultivar Remus and its resistant near-isogenic line NIL3 carrying the entire Qfhs.ifa-5A segment. By manually removing anthers prior to spray inoculation both, Remus and NIL3 became almost equally resistant in the early phase of the disease development and were significantly less diseased than variants without anther manipulation. At late time points the positive effect of the anther removal became smaller for Remus and disappeared completely for NIL3. Results affirm that absence of anthers enhanced resistance to initial infection but did not protect plants from fungal spreading within spikes.
| S-EPMC6588648 | biostudies-literature
Project description:Watermelon fruit texture and quality are determined by flesh firmness. As a quality trait, flesh firmness is controlled by multigenes. Defining the key regulatory factors of watermelon flesh firmness is of great significance for watermelon genetic breeding. In this study, the hard-flesh egusi seed watermelon PI186490 was used as the male parent, the soft-flesh cultivated watermelon W1-1 was used as the female parent, and 175 F2 generations were obtained from selfing F1. Primary mapping of the major genes controlling center flesh firmness was achieved by bulked-segregant analysis (BSA)-Seq analysis and molecular marker technology. Finally, major genes were delimited in the physical interval between 6,210,787 and 7,742,559 bp on chromosome 2 and between 207,553 and 403,137 bp on chromosome 8. The content of each cell wall component and hormone was measured, and comparative transcriptome analysis was performed during fruit development in watermelon. The protopectin, cellulose, hemicellulose, indole-3-acetic acid (IAA) and abscisic acid (ABA) contents were measured, and paraffin sections were made during the three fruit developmental stages. The results revealed that protopectin, celluloses, and hemicelluloses exhibited similar trends for flesh firmness, while the IAA and ABA concentrations continued to decrease with fruit ripening. Paraffin sections showed that PI186490 cells were more numerous, were more tightly packed, had clearer cell wall edges and had thicker cell walls than W1-1 cells at every developmental stage. Comparative transcriptome analysis was conducted on RNA samples of flesh during fruit development and ripening in W1-1 and PI186490. The results from the localization interval transcriptome analysis showed that Cla016033 (DUF579 family member), which may influence the cell wall component contents to adjust the flesh firmness in watermelon fruit, was different in W1-1 and PI186490 and that Cla012507 (MADS-box transcription factor) may be involved in the regulation of fruit ripening and affect the hardness of watermelon fruit.
| S-EPMC7308538 | biostudies-literature
Project description:BACKGROUND: Common bacterial blight (CBB), incited by Xanthomonas axonopodis pv. phaseoli (Xap), is a major yield-limiting factor of common bean (Phaseolus vulgaris L.) production around the world. Host resistance is practically the most effective and environmentally-sound approach to control CBB. Unlike conventional QTL discovery strategies, in which bi-parental populations (F2, RIL, or DH) need to be developed, association mapping-based strategies can use plant breeding populations to synchronize QTL discovery and cultivar development. RESULTS: A population of 469 dry bean lines of different market classes representing plant materials routinely developed in a bean breeding program were used. Of them, 395 lines were evaluated for CBB resistance at 14 and 21 DAI (Days After Inoculation) in the summer of 2009 in an artificially inoculated CBB nursery in south-western Ontario. All lines were genotyped using 132 SNPs (Single Nucleotide Polymorphisms) evenly distributed across the genome. Of the 132 SNPs, 26 SNPs had more than 20% missing data, 12 SNPs were monomorphic, and 17 SNPs had a MAF (Minor Allelic Frequency) of less than 0.20, therefore only 75 SNPs were used for association study, based on one SNP per locus. The best possible population structure was to assign 36% and 64% of the lines into Andean and Mesoamerican subgroups, respectively. Kinship analysis also revealed complex familial relationships among all lines, which corresponds with the known pedigree history. MLM (Mixed Linear Model) analysis, including population structure and kinship, was used to discover marker-trait associations. Eighteen and 22 markers were significantly associated with CBB rating at 14 and 21 DAI, respectively. Fourteen markers were significant for both dates and the markers UBC420, SU91, g321, g471, and g796 were highly significant (p ? 0.001). Furthermore, 12 significant SNP markers were co-localized with or close to the CBB-QTLs identified previously in bi-parental QTL mapping studies. CONCLUSIONS: This study demonstrated that association mapping using a reasonable number of markers, distributed across the genome and with application of plant materials that are routinely developed in a plant breeding program can detect significant QTLs for traits of interest.
| S-EPMC3078875 | biostudies-literature
Project description:Key messageThe QTL Fhb1 was successfully introgressed and validated in three durum wheat populations. The novel germplasm and the QTL detected will support improvement of Fusarium resistance in durum wheat. Durum wheat (Triticum durum Desf.) is particularly susceptible to Fusarium head blight (FHB) and breeding for resistance is hampered by limited genetic variation within this species. To date, resistant sources are mainly available in a few wild relative tetraploid wheat accessions. In this study, the effect of the well-known hexaploid wheat (Triticum aestivum L.) quantitative trait locus (QTL) Fhb1 was assessed for the first time in durum wheat. Three F7-RIL mapping populations of about 100 lines were developed from crosses between the durum wheat experimental line DBC-480, which carries an Fhb1 introgression from Sumai-3, and the European T. durum cultivars Karur, Durobonus and SZD1029K. The RILs were evaluated in field experiments for FHB resistance in three seasons using spray inoculation and genotyped with SSR as well as genotyping-by-sequencing markers. QTL associated with FHB resistance were identified on chromosome arms 2BL, 3BS, 4AL, 4BS, 5AL and 6AS at which the resistant parent DBC-480 contributed the positive alleles. The QTL on 3BS was detected in all three populations centered at the Fhb1 interval. The Rht-B1 locus governing plant height was found to have a strong effect in modulating FHB severity in all populations. The negative effect of the semi-dwarf allele Rht-B1b on FHB resistance was compensated by combining with Fhb1 and additional resistance QTL. The successful deployment of Fhb1 in T. durum was further substantiated by assessing type 2 resistance in one population. The efficient introgression of Fhb1 represents a significant step forward for enhancing FHB resistance in durum wheat.
| S-EPMC5215227 | biostudies-literature
Project description:Breeding for Fusarium head blight (FHB) resistance in durum wheat is complicated by the quantitative trait expression and narrow genetic diversity of available resources. High-density mapping of the FHB resistance quantitative trait loci (QTL), evaluation of their co-localization with plant height and maturity QTL and the interaction among the identified QTL are the objectives of this study. Two doubled haploid (DH) populations, one developed from crosses between Triticum turgidum ssp. durum lines DT707 and DT696 and the other between T. turgidum ssp. durum cv. Strongfield and T. turgidum ssp. carthlicum cv. Blackbird were genotyped using the 90K Infinium iSelect chip and evaluated phenotypically at multiple field FHB nurseries over years. A moderate broad-sense heritability indicated a genotype-by-environment interaction for the expression of FHB resistance in both populations. Resistance QTL were identified for the DT707 × DT696 population on chromosomes 1B, 2B, 5A (two loci) and 7A and for the Strongfield × Blackbird population on chromosomes 1A, 2A, 2B, 3A, 6A, 6B and 7B with the QTL on chromosome 1A and those on chromosome 5A being more consistently expressed over environments. FHB resistance co-located with plant height and maturity QTL on chromosome 5A and with a maturity QTL on chromosome 7A for the DT707 × DT696 population. Resistance also co-located with plant height QTL on chromosomes 2A and 3A and with maturity QTL on chromosomes 1A and 7B for the Strongfield × Blackbird population. Additive × additive interactions were identified, for example between the two FHB resistance QTL on chromosome 5A for the DT707 × DT696 population and the FHB resistance QTL on chromosomes 1A and 7B for the Strongfield × Blackbird population. Application of the Single Nucleotide Polymorphic (SNP) markers associated with FHB resistance QTL identified in this study will accelerate combining genes from the two populations.
| S-EPMC6181299 | biostudies-literature