RESUMO
The melon fruit surface groove (fsg) not only affects peel structure and causes stress-induced fruit cracking but also fits consumers' requirements in different regions. In this study, genetic inheritance analysis of three F2 populations derived from six parental lines revealed that the fsg trait is controlled by a simple recessive inherited gene. Through bulked segregant analysis sequencing (BSA-seq), the Cmfsg locus was detected in an 8.96 Mb interval on chromosome 11 and then initially mapped to a region of approximately 1.15 Mb. Further fine mapping with a large F2 population including 1,200 plants narrowed this region to 207 kb containing 11 genes. A genome-wide association study (GWAS) with 187 melon accessions also produced the same chromosome region for the Cmfsg locus. Due to the rare molecular markers and lack of mutations in the coding and promoter regions of the 11 candidate genes in the fine-mapped interval, we conducted in silico BSA to explore the natural melon panel to predict candidate genes for the Cmfsg locus. A 1.07 kb segment upstream of MELO3C019694.2 (annotated as the AGAMOUS MADS-box transcription factor) exhibited a correlation with the grooved and non-grooved accessions among the F2 individuals, and a natural panel consisted of 17 melon accessions. The expression level of MELO3C019694.2 in the pericarp was higher in grooved lines than in non-grooved lines and was specifically expressed in fruit compared with other tissues (female flower, male flower, root, and leaf). This work provides fundamental information for further research on melon fsg trait formation and molecular markers for melon breeding.
RESUMO
Fruit pedicel (FP) is an important determinant of premium fruit quality that directly affects commercial market value. However, in-depth molecular and genetic basis of pedicel-related traits has not been identified in watermelon. Herein, a quantitative trait locus (QTL) mapping strategy was used to identify the potential genetic regions controlling FP traits based on newly derived whole-genome single nucleotide polymorphism based cleaved amplified polymorphism sequence (SNP-CAPS) markers. Next-generation sequencing based whole-genome re-sequencing of two watermelon parent lines revealed 98.30 and 98.40% of average coverage, 4,989,869 SNP variants, and 182,949 CAPS loci pairs across the reference genome, respectively. A total of 221 sets of codominant markers exhibited 46.42% polymorphism rate and were effectively genotyped within 100-F2:3 derived mapping population. The developed linkage map covered a total of 2,630.49 cM genetic length with averaged 11.90 cM, and depicted a valid marker-trait association. In total, 6 QTLs (qFPL4.1, qFPW4.1, qFPD2.1, qFPD2.2, qFPD8.1, qFPD10.1) were mapped with five major effects and one minor effect between the whole genome adjacent markers positioned over distinct chromosomes (02, 04, 08, 10), based on the ICIM-ADD mapping approach. These significant QTLs were similarly mapped in delimited flanking regions of 675.10, 751.38, 859.24, 948.39, and 947.51 kb, which collectively explained 8.64-13.60% PVE, respectively. A highly significant and positive correlation was found among the observed variables. To our knowledge, we first time reported the mapped QTLs/genes affecting FP traits of watermelon, and our illustrated outcomes will deliver the potential insights for fine genetic mapping as well as functional gene analysis through MAS-based breeding approaches.
RESUMO
Folate metabolism plays quite a critical role in Parkinson's disease (PD). Previous published research works have studied the link existing between the folate metabolism genetic polymorphisms and PD susceptibility; nevertheless, the results continue having controversies and inconclusiveness. Accordingly, we carried out the present meta-analysis for the assessment of the potential link between the folate metabolism genetic polymorphisms and the susceptibility to PD. In addition we carried out a literature search in the PubMed, EMBASE, Cochrane Library, and WanFang databases till November 10, 2018. The odds ratios (ORs) with corresponding 95% credible interval (95%CI) were put to use for evaluating the strength of the association of three folate metabolism genetic polymorphism ( C677T, A1298C, and A2756G) with the susceptibility to PD. Each statistical analysis was carried out with the use of STATA 15.0. An aggregate of twenty-one case-control investigations were retrieved, which involved 3,944 PD patients and 4,412 controls. We discovered the existence of no substantial link between the C677T and A1298C polymorphism and PD risk in any genetic framework comparisons. With regard to A2756G polymorphism, we discovered that there was an association between the A2756G genetic polymorphism and an augmented threat of PD in the co-dominant genetic framework (GG vs. AA: OR=1.86, 95%CI=1.02-3.37, P=0.042) and the recessive genetic model (GG vs. GA+AA: OR=1.90, 95%CI=1.06-3.41, P=0.031). To summarize, our research work indicates that the A2756G polymorphism of the folate metabolism gene had an association with an augmented threat of PD. Also, A1298C polymorphisms is unlikely to significantly contribute towards the susceptibility to PD. Further large-scale case-control studies are still required.