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Glia to axon RNA transfer
Author(s) -
Sotelo José Roberto,
Canclini Lucía,
Kun Alejandra,
SoteloSilveira José Roberto,
Calliari Aldo,
Cal Karina,
Bresque Mariana,
DiPaolo Andrés,
Farias Joaquina,
Mercer John A.
Publication year - 2014
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.22125
Subject(s) - axon , biology , soma , neuroscience , ribosome , rna , axoplasmic transport , neurodegeneration , microbiology and biotechnology , genetics , gene , pathology , medicine , disease
ABSTRACT The existence of RNA in axons has been a matter of dispute for decades. Evidence for RNA and ribosomes has now accumulated to a point at which it is difficult to question, much of the disputes turned to the origin of these axonal RNAs. In this review, we focus on studies addressing the origin of axonal RNAs and ribosomes. The neuronal soma as the source of most axonal RNAs has been demonstrated and is indisputable. However, the surrounding glial cells may be a supplemental source of axonal RNAs, a matter scarcely investigated in the literature. Here, we review the few papers that have demonstrated that glial‐to‐axon RNA transfer is not only feasible, but likely. We describe this process in both invertebrate axons and vertebrate axons. Schwann cell to axon ribosomes transfer was conclusively demonstrated (Court et al. [2008]: J. Neurosci 28:11024–11029; Court et al. [2011]: Glia 59:1529–1539). However, mRNA transfer still remains to be demonstrated in a conclusive way. The intercellular transport of mRNA has interesting implications, particularly with respect to the integration of glial and axonal function. This evolving field is likely to impact our understanding of the cell biology of the axon in both normal and pathological conditions. Most importantly, if the synthesis of proteins in the axon can be controlled by interacting glia, the possibilities for clinical interventions in injury and neurodegeneration are greatly increased. © 2013 Wiley Periodicals, Inc. Develop Neurobiol 74: 292–302, 2014

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