The origin of cultivated tree peonies, known as the ‘king of flowers' in China for more than 1000 years, has attracted considerable interest, but remained unsolved. Here, we conducted phylogenetic analyses of explicitly sampled traditional cultivars of tree peonies and all wild species from the shrubby section Moutan of the genus Paeonia based on sequences of 14 fast-evolved chloroplast regions and 25 presumably single-copy nuclear markers identified from RNA-seq data. The phylogeny of the wild species inferred from the nuclear markers was fully resolved and largely congruent with morphology and classification. The incongruence between the nuclear and chloroplast trees suggested that there had been gene flow between the wild species. The comparison of nuclear and chloroplast phylogenies including cultivars showed that the cultivated tree peonies originated from homoploid hybridization among five wild species. Since the origin, thousands of cultivated varieties have spread worldwide, whereas four parental species are currently endangered or on the verge of extinction. The documentation of extensive homoploid hybridization involved in tree peony domestication provides new insights into the mechanisms underlying the origins of garden ornamentals and the way of preserving natural genetic resources through domestication.
Seven dihydrochalcone compounds were isolated from the leaves of Malus crabapples, cv. "Radiant", and their chemical structures were elucidated by UV, IR, ESI-MS, 1 H-NMR and 13 C-NMR analyses. These compounds, which include trilobatin (A1), phloretin (A2), 3-hydroxyphloretin (A3), phloretin rutinoside (A4), phlorizin (A5), 6 11 -O-coumaroyl-4 1 -O-glucopyranosylphloretin (A6), and 3 111 -methoxy-6 11 -O-feruloy-4 1 -O-glucopyranosyl-phloretin (A7), all belong to the phloretin class and its derivatives. Compounds A6 and A7 are two new rare dihydrochalcone compounds. The results of a MTT cancer cell growth inhibition assay demonstrated that phloretin and these derivatives showed significant positive anticancer activities against several human cancer cell lines, including the A549 human lung cancer cell line, Bel 7402 liver cancer cell line, HepG2 human ileocecal cancer cell line, and HT-29 human colon cancer cell line. A7 had significant effects on all cancer cell lines, suggesting potential applications for phloretin and its derivatives. Adding a methoxyl group to phloretin dramatically increases phloretin's anticancer activity.
Citrus species are among the most important fruit trees in the world and have a long cultivation history. However, until now, the exact genetic origins of cultivated Citrus such as sweet orange (Citrus sinensis), lemon (C. limon), and grapefruit (C. paradisi) have remained unidentified. In the present study, amplified fragment length polymorphism (AFLP) fingerprints, nuclear internal transcribed spacer (ITS), and three plastid DNA regions (psbH – petB, trnL – trnF, and trnS - trnG) of 30 accessions of the cultivated citrus and their putative wild ancestors were analyzed in an attempt to identify their paternal and maternal origins. Molecular phylogenetic trees were constructed based on the AFLP data, and chloroplast DNA and ITS sequences using the genus Poncirus as the outgroup. Our results indicated that bergamot (C. aurantifolia) and lemon were derived from citron (C. medica) and sour orange (C. aurantium), and grapefruit was a hybrid that originated from a cross between pummelo (C. grandis) and sweet orange. Rough lemon (C. limon) was probable as a parent of rangpur lime (C. limonia) and guangxi local lemon (C. limonia). Our data also demonstrated that sweet orange and sour orange were hybrids of mandarin (C. reticulata) and pummelo, while rough lemon was a cross between citron and mandarin. For mexican lime (C. aurantifolia), our molecular data confirmed a species of Papeda to be the female parent and C. medica as the male. These findings provide new information for future study on the taxonomy, evolution, and genetic breeding of Citrus.
microRNAs (miRNAs) are involved in the regulation of almost all physiological and pathological processes, including osteoblast proliferation and differentiation. miR-375 has been reported to be aberrantly expressed in various tumor types and to inhibit cell proliferation and invasion by targeting a number of key genes. However, the effects of miR-375 on osteogenic differentiation have not been investigated. Thus, the present study aimed to elucidate the function served by miR-375 in osteogenic differentiation. The expression levels of miR-375 were observed to decrease in a C2C12 cell model of osteogenic differentiation. Overexpression of miR-375 inhibited the activity of key osteoblast markers, including osteocalcin (OC), alkaline phosphatase (ALP) and collagen, type I, α 1 (COL1A1). By contrast, inhibition of miR-375 expression resulted in an increase in the osteogenic potential, as indicated by the enhanced expression levels of OC, ALP and COL1A1. In addition, a dual-luciferase reporter assay indicated that runt-related transcription factor 2 (RUNX2) was a target of miR-375. Western blot analysis revealed that the inhibition of miR-375 led to a significant increase in the protein expression levels of RUNX2. In addition, overexpression of RUNX2 was observed to attenuate the miR-375-mediated suppression of osteogenic differentiation. Therefore, the results demonstrated that miR-375 was able to inhibit osteogenic differentiation via the regulation of RUNX2 expression.
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