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Novel RNA- and FMRP-binding protein TRF2-S regulates axonal mRNA transport and presynaptic plasticity.

Authors: Zhang, Peisu  Abdelmohsen, Kotb  Liu, Yong  Tominaga-Yamanaka, Kumiko  Yoon, Je-Hyun  Ioannis, Grammatikakis  Martindale, Jennifer L  Zhang, Yongqing  Becker, Kevin G  Yang, In Hong  Gorospe, Myriam  Mattson, Mark P 
Citation: Zhang P, etal., Nat Commun. 2015 Nov 20;6:8888. doi: 10.1038/ncomms9888.
Pubmed: (View Article at PubMed) PMID:26586091
DOI: Full-text: DOI:10.1038/ncomms9888

Despite considerable evidence that RNA-binding proteins (RBPs) regulate mRNA transport and local translation in dendrites, roles for axonal RBPs are poorly understood. Here we demonstrate that a non-telomeric isoform of telomere repeat-binding factor 2 (TRF2-S) is a novel RBP that regulates axonal plasticity. TRF2-S interacts directly with target mRNAs to facilitate their axonal delivery. The process is antagonized by fragile X mental retardation protein (FMRP). Distinct from the current RNA-binding model of FMRP, we show that FMRP occupies the GAR domain of TRF2-S protein to block the assembly of TRF2-S-mRNA complexes. Overexpressing TRF2-S and silencing FMRP promotes mRNA entry to axons and enhances axonal outgrowth and neurotransmitter release from presynaptic terminals. Our findings suggest a pivotal role for TRF2-S in an axonal mRNA localization pathway that enhances axon outgrowth and neurotransmitter release.


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CRRD Object Information
CRRD ID: 13702251
Created: 2018-07-18
Species: All species
Last Modified: 2018-07-18
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.