Journal
JOURNAL OF NEUROSCIENCE
Volume 33, Issue 37, Pages 14666-U65Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.4821-12.2013
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Funding
- National Science Foundation [IOS 951043, IOS 1257449]
- American Association of University Women Fellowship
- Sigma Xi
- Division Of Integrative Organismal Systems
- Direct For Biological Sciences [0951043, 1257449] Funding Source: National Science Foundation
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c-Jun N-terminal kinase (JNK) mediates cell signaling essential for axon outgrowth, but the associated substrates and underlying mechanisms are poorly understood. We identified in Xenopus laevis embryos a novel posttranscriptional mechanism whereby JNK regulates axonogenesis by phosphorylating a specific site on heterogeneous nuclear ribonucleoprotein K (hnRNP K). Both JNK inhibition and hnRNP K knockdown inhibited axon outgrowth and translation of hnRNP K-regulated cytoskeletal RNAs (tau and neurofilament medium), effects that were alleviated by expressing phosphomimetic, but not phosphodeficient, forms of hnRNP K. Immunohistochemical and biochemical analyses indicated that JNK phosphorylation of hnRNP K occurred within the cytoplasm and was necessary for the translational initiation of hnRNP K-targeted RNAs but not for hnRNP K intracellular localization or RNA binding. Thus, in addition to its known roles in transcription and cytoskeletal organization, JNK acts posttranscriptionally through hnRNP K to regulate translation of proteins crucial for axonogenesis.
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