RÉSUMÉ
The aims of this study were to establish a random amplified polymorphic DNA (RAPD) fingerprint database of chloroplast DNA (cpDNA) from different cultivars of Cornus officinalis and to convert RAPD markers to sequence characterized amplified regions (SCAR) markers. A method of extraction was established that was suitable for obtaining cpDNA from samples rapidly dried in silicone; an RAPD fingerprint database was built; and the genetic distance between samples was used as statistical clustering variables for calculating DICE genetic similarity coefficients and for building a kinship tree chart. RAPD markers were converted to SCAR markers to design specific primers, and samples from C. officinalis cultivars, plants of the same family, and its adulterants, were used for amplification and identification. Fifteen amplified primers with stable polymorphisms were screened for amplification of 130 copies of materials. In total, 57 sites were achieved, 40 of which were polymorphic, and the polymorphic rate was up to 70.18%. A genetic tree was built based on seven cultivars. SCAR markers of C. officinalis cpDNA were successfully converted into RAPD markers. cpDNA samples from hawthorn, C. officinalis, Cornus wood, and grape were used for SCAR amplification, and their bands were distinctly different. In conclusion, SCAR markers and cpDNA may be used for research on C. officinalis and its adulterants, and the results may provide a basis for identifying germplasm and screening fine varieties at a molecular level.
Sujet(s)
Cornus/génétique , ADN des chloroplastes/génétique , Marqueurs génétiques , Polymorphisme génétique , Séquence nucléotidique , Analyse de regroupements , Cornus/classification , ADN des chloroplastes/composition chimique , Données de séquences moléculaires , Technique RAPD , Analyse de séquence d'ADN , Transformation génétiqueRÉSUMÉ
The aim of this study was to determine whether single nucleotide polymorphisms (SNPs) in APM1 contribute to disorders of lipid metabolism in hypertensive disorder complicating pregnancy (HDCP). The study included 178 pregnant women with HDCP and 243 healthy pregnant controls. Using PCR-restriction fragment length polymorphism, we detected the frequencies of genotypes, alleles, and haplotypes of two SNPs, +45T>G (rs2241766) and +276G>T (rs1501299), in APM1. We found that the SNP +276 TT genotype was significantly associated with protection against HDCP compared to the pooled G genotypes. The genotype and allele frequency distributions of SNP +276 were significantly different between the cases and controls. Single-point genotype and allele distributions in SNP +45 were not statistically different between the groups. The pooled G haplotypes were significantly overrepresented in the case group compared to the TT haplotype. Plasma adiponectin (APN) concentration was determined by enzyme-linked immunosorbent assay, and we found that APN levels in cases were significantly lower than those in controls. Using the clinical data, we evaluated the correlation between the two SNPs and HDCP development, and revealed an association between the two SNPs and disorders of lipid metabolism in patients with HDCP. Except for fasting insulin levels, which was higher in cases than in controls, there were no significant differences in the other clinical data between the two groups.