McDermott, John Charles2019-07-022019-07-022019-04-052019-07-02http://hdl.handle.net/10315/36313Skeletal muscle consists of multinucleated myofibers which generate contractile force and regulate glucose levels in the human body. Over time, skeletal muscle can become damaged and therefore requires a robust capacity to self-renew. One of the emerging areas of skeletal muscle research involves studying the post-transcriptional mechanisms of gene regulation which mediate this self-renewal pathway. In this study we present the role of the -catenin-FMRP complex in skeletal muscle. First, we confirmed that -catenin and FMRP interacted through biochemical assays and overexpression of -catenin and FMRP fluorescent fusion proteins. Next, we found that knockdown of -catenin in C2C12 myoblasts undergoing the growth phase led to a significant increase in global translational activity. Finally we identified the presence of -catenin at the translational machinery. In conclusion, this study suggests that the -catenin-FMRP complex may serve as a potential pharmacological target in muscle wasting disorders where protein synthesis is greatly impaired.enAuthor owns copyright, except where explicitly noted. Please contact the author directly with licensing requests.Electronic Thesis or Dissertation2019-07-02Skeletal muscleBiologyFragile X Mental Retardation ProteinFMRPβ-cateninBeta-catenintranslationpost-transcriptionalmyofiberC2C12 myoblast