Journal
JOURNAL OF NEUROSCIENCE
Volume 32, Issue 14, Pages 4944-4958Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5868-11.2012
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Funding
- Instituto de Salud Carlos III (FIS) [PS09/00094]
- Fundacion Cientifica de la Asociacion Espanola Contra el Cancer
- Ministry of Science and Innovation, Spain
- Royal Society of Great Britain
- National Institutes of Health [AT-1576]
- Spanish Ministry of Science [SAF2011-29851]
- Sanidad Gobierno Vasco
- Educacion Gobierno Vasco
- Instituto de Salud Carlos III
- National Institute on Aging, National Institutes of Health
- [PI11/01588]
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An important prerequisite to myelination in peripheral nerves is the establishment of one-to-one relationships between axons and Schwann cells. This patterning event depends on immature Schwann cell proliferation, apoptosis, and morphogenesis, which are governed by coordinated changes in gene expression. Here, we found that the RNA-binding protein human antigen R (HuR) was highly expressed in immature Schwann cells, where genome-wide identification of its target mRNAs in vivo in mouse sciatic nerves using ribonomics showed an enrichment of functionally related genes regulating these processes. HuR coordinately regulated expression of several genes to promote proliferation, apoptosis, and morphogenesis in rat Schwann cells, in response to NRG1, TGF beta, and laminins, three major signals implicated in this patterning event. Strikingly, HuR also binds to several mRNAs encoding myelination-related proteins but, contrary to its typical function, negatively regulated their expression, likely to prevent ectopic myelination during development. These functions of HuR correlated with its abundance and subcellular localization, which were regulated by different signals in Schwann cells.
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