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Journal Article

The sirtuin SIRT6 regulates stress granule formation in C. elegans and mammals.

MPS-Authors
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Jedrusik-Bode,  M. A.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

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Studencka,  M.
Department of Genes and Behavior, MPI for biophysical chemistry, Max Planck Society;

External Resource

http://jcs.biologists.org/content/126/22/5166.full.pdf+html
(Publisher version)

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Fulltext (public)

1868229.pdf
(Publisher version), 4MB

Supplementary Material (public)

1868229_Suppl_1.pdf
(Supplementary material), 6MB

Citation

Jedrusik-Bode, M. A., Studencka, M., Smolka, C., Baumann, T., Schmidt, H., Kampf, J., et al. (2013). The sirtuin SIRT6 regulates stress granule formation in C. elegans and mammals. Journal of Cell Science, 126, 5166-5177. doi:10.1242/jcs.130708.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0014-C701-9
Abstract
SIRT6 is a NAD+-dependent deacetylase that modulates chromatin structure and safeguards genomic stability. Until now, SIRT6 has been assigned to the nucleus and only nuclear targets of SIRT6 are known. Here, we demonstrate that in response to stress, C. elegans SIR-2.4 and its mammalian orthologue SIRT6 localize to cytoplasmic stress granules, interact with various stress granule components and induce their assembly. Loss of SIRT6 or inhibition of its catalytic activity in mouse embryonic fibroblasts impairs stress granule formation and delays disassembly during recovery, whereas deficiency of SIR-2.4 diminishes maintenance of P granules and decreases survival of C. elegans under stress conditions. Our findings uncover a novel, evolutionary conserved function of SIRT6 in the maintenance of stress granules in response to stress.