The Ceman Lab is working with the molecular basis of disease, post-translational modifications, regulation of RNA expression, and RNA-protein interactions surrounding Fragile X Syndrome. More specifically, we are interested in how FMRP recruits Ago2 to microRNA recognition elements (MREs) in the 3’UTR of its target mRNAs. Our long-term goal is to uncover the mechanism of FMRP-mediated translation regulation, exploring both associated proteins and microRNAs.

What is FMRP and Why Study it?

The fragile X mental retardation protein FMRP is required for normal cognition: when it is absent, the most common form of inherited mental retardation, fragile X syndrome (FXS) results. Thus, FMRP is a molecular entry point for understanding normal neuronal function. FMRP is an RNA binding protein that binds ~4% of brain mRNAs and regulates their expression—either enhancing or suppressing translation by an unknown mechanism. Many of the mRNAs that bind FMRP have been identified; however, it is still unknown how FMRP regulates their translation. FMRP also directly binds the RNA helicase Mov10, which unwinds mRNAs to reveal MREs.

We are also interested in studying Mov10’s role in the brain. We know that it is expressed throughout the brain. We also know that when Mov10 expression is reduced by half, dendritic arborization is compromised.

Our Principal Investigator is Stephanie Ceman.

Check out at our website here.