拟黑多刺蚁肌细胞增强因子2(MEF2)生物信息学分析

应用NCBI上的常用程序、ExPASy在线核苷酸序列分析工具、CBS生物学序列分析工具及SABLE在线分析软件等对拟黑多刺蚁Polyrhachi svicina Roger肌细胞增强因子2(PvMEF2)进行了生物信息学分析,获得了PvMEF2因子的序列特征及理化性质,并对其结构和功能结构域进行了预测。结果表明PvMEF2因子具有与已知种类MEF2因子较高一致性的MADS和MEF2结构域,并且理化性质和二级结构、三级结构等与果蝇该因子类似,反映了PvMEF2可能是参与拟黑多刺蚁肌肉发生调控的重要因子。     

Overexpression of CUG triplet repeat-binding protein, CUGBP1, in mice inhibits myogenesis

Accumulation of RNA CUG repeats in myotonic dystrophy type 1 (DM1) patients leads to the induction of a CUG-binding protein, CUGBP1, which increases translation of several proteins that are required for myogenesis. In this paper, we examine the role of overexpression of CUGBP1 in DM1 muscle pathology using transgenic mice that overexpress CUGBP1 in skeletal muscle. Our data demonstrate that the elevation of CUGBP1 in skeletal muscle causes overexpression of MEF2A and p21 to levels that are significantly higher than those in skeletal muscle of wild type animals. A similar induction of these proteins is observed in skeletal muscle of DM1 patients with increased levels of CUGBP1. Immunohistological analysis showed that the skeletal muscle from mice overexpressing CUGBP1 is characterized by a developmental delay, muscular dystrophy, and myofiber-type switch: increase of slow/oxidative fibers and the reduction of fast fibers. Examination of molecular mechanisms by which CUGBP1 up-regulates MEF2A shows that CUGBP1 increases translation of MEF2A via direct interaction with GCN repeats located within MEF2A mRNA. Our data suggest that CUGBP1-mediated overexpression of MEF2A and p21 inhibits myogenesis and contributes to the development of muscle deficiency in DM1 patients.