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Multiple mechanisms repress N-Bak mRNA translation in the healthy and apoptotic neurons

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Jakobson,  M.
Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Jakobson, M., Jakobson, M., Llano, O., Palgi, J., & Arumae, U. (2013). Multiple mechanisms repress N-Bak mRNA translation in the healthy and apoptotic neurons. CELL DEATH & DISEASE, 4: e777. doi:10.1038/cddis.2013.297.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-67B3-E
Abstract
N-Bak is a neuron-specific BH3-only splice variant of pro-apoptotic Bcl-2 family member Bak. We have shown that its mRNA is stable in the neurons, whereas the protein cannot be detected by antibodies, suggesting a strong translational arrest of the mRNA. Here we identify two regulatory elements in the N-Bak mRNA that significantly repress translation in the luciferase reporter assay: an upstream open reading frame in the 5'-untranslated region (UTR) and naturally spliced exon-exon junction downstream of the premature translation termination codon in the 3'UTR. We also show that N-Bak mRNA is stored in granular structures in the sympathetic neurons and stays in these granules during intrinsic apoptosis. Finally, we confirm the absence of N-Bak protein by quantitative mass spectrometry analysis in the healthy, apoptotic or stressed sympathetic and cortical neurons. We conclude that N-Bak mRNA is translationally repressed by multiple mechanisms, and the protein does not participate in the classical apoptosis or cellular stress response.