[Molecular mechanisms of meiotic recombination suppression in plants].

Meiotic recombination not only ensures the stability of chromosome numbers during the sexual reproduction in eukaryotes, but also shuffles the maternal and paternal genetic materials to generate genetic diversity in the gametes. Therefore, meiotic recombination is an important pathway for genetic diversity, which has been considered as a major driving force for species evolution and biodiversity in nature. In most eukaryotes, meiotic recombination is strictly limited, despite the large variation of physical genome size and chromosome numbers among species, but the mechanisms suppressing meiotic recombination remain elusive. Recently, several suppressors have been identified through the forward genetics screen, and revealed the functions and regulation pathways of these suppressors. In this review, we summarize the breakthrough discovery of meiotic recombination suppressors in plants based on research in Arabidopsis, with particular focus on the gene function and its regulation network to elucidate the molecular mechanisms of meiotic recombination suppression in plants.

Biocompatibility and in vivo osteogenic capability of novel bone tissue engineering scaffold A-W-MGC/CS.

BACKGROUND: This study aims to investigate the biocompatibility and in vivo osteogenic capability of the novel bone tissue engineering scaffold apatite-wollastonite-magnetic glass ceramic/chitosan (A-W-MGC/CS). METHODS: Rabbit bone marrow stromal cells (BMSCs) were transfected with adenovirus-human bone morphogenetic protein-2-green fluorescent protein (Ad-hBMP2-GFP). The transfected BMSCs were then inoculated onto the scaffold material A-W-MGC/CS to construct tissue-engineered bone. The attachment and proliferation of BMSCs were observed by scanning electron microscopy (SEM) and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) detection, respectively. Rabbit models of bone defects were established and divided into three groups. Experimental group 1 was implanted with prepared tissue-engineered bone. Experimental group 2 was implanted with A-W-MGC/CS without transfected BMSCs. The blank group was injected with transfected BMSCs, without implantation of any scaffold. In the 12th week after surgery, the repair of bone defect was observed by X-ray examination, and histological observations of the area of bone defect were performed. RESULTS: A-W-MGC/CS resulted in good BMSC attachment and had no obvious effects on cell proliferation. In experimental group 1, good repair of bone defect was observed, and the scaffold material degraded completely. In experimental group 2, new bone was formed, but its quality was poor. In the blank group, there was mainly filling of fibrous connective tissues with no observable bone defect repair. CONCLUSION: A-W-MGC/CS possesses good biocompatibility and in vivo osteogenic capability for bone defect repair.