ABSTRACT
Lycophytes and seed plants constitute the typical vascular plants. Lycophytes have been thought to have no paleo-polyploidization although the event is known to be critical for the fast expansion of seed plants. Here, genomic analyses including the homologous gene dot plot analysis detected multiple paleo-polyploidization events, with one occurring approximately 13-15 million years ago (MYA) and another about 125-142 MYA, during the evolution of the genome of Selaginella moellendorffii, a model lycophyte. In addition, comparative analysis of reconstructed ancestral genomes of lycophytes and angiosperms suggested that lycophytes were affected by more paleo-polyploidization events than seed plants. Results from the present genomic analyses indicate that paleo-polyploidization has contributed to the successful establishment of both lineages-lycophytes and seed plants-of vascular plants.
Subject(s)
Evolution, Molecular , Genome, Plant , Genomics , Phylogeny , Polyploidy , Selaginellaceae/geneticsABSTRACT
<p><b>OBJECTIVE</b>To screen the most strong emodin derivative inhibiting the proliferation of multiple myeloma(MM) cells and to explore the inhibitory and inducing effects of emodin derivatives on proliferation and apoptosis of MM cell lines RPMI 8226 and U266.</p><p><b>METHODS</b>Sixteen emodin derivatives were designed and synthesized by using emodin as mother substance, then from which the emodin derivative E11 was screened for experiments. The MTT method and cell colony formation assay were used to observe the effect of E11 on proliferation of RPMI 8226 and U266, the fluorescent microscopy with DAFI staining was used to observed the morphological changes of MM cells treated with emodin dervative 11, the DNA fragmentation detection was used to detect the inducing apoptosis effect of E11 on RPMI 8226 and U266 cells treated with E11.</p><p><b>RESULTS</b>The MTT assay showed that after the RPMI 8226 cells were treated with 16 kinds of emodin derivatives for 48 hours, the 50% inhibition concentration（IC） of 14 emodin dervatives was between 0.83-34.68 µmol/L, except E10 and E15 because their IC could not be calculated. The IC of E11 for RPMI 8226 and U266 cells were 0.831±0.0453 µmol/L and 1.039±0.093 µmol/L, respectively. Cell colony formation assay showed that E11 could inhibit RPMI8226 and U266 cells' colony formation in dose-.and time- dependent manner (r=0.72). Cell apoptosis was observed in RPMI8226 and U266 cells by DAPI staining , and also by the detection of DNA fragmentation.</p><p><b>CONCLUSION</b>In the synthesis of 16 kinds of emodin derivatives, the inhibitory effect of E11 on prolife-ration of RPMI8226 cell was the strongest. E11 can remarkably inhibit proliferation and induce apoptosis of RPMI8226 and U266 cells.</p>