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Journal Article

Ataxin-2-like is a regulator of stress granules and processing bodies

MPS-Authors
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Kähler,  Christian
Neurodegenerative Disorders (Sylvia Krobitsch), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Isensee,  Jörg
Signal Transduction in Mental Retardation and Pain (Tim Hucho), Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;
Universitätsklinik Köln, Klinik für Anästhesiologie und Operative Intensivmedizin, Experimentelle Anästhesiologie und Schmerzforschung;

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Nonhoff,  Ute
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Hucho,  Tim
Signal Transduction in Mental Retardation and Pain (Tim Hucho), Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;
Universitätsklinik Köln, Klinik für Anästhesiologie und Operative Intensivmedizin, Experimentelle Anästhesiologie und Schmerzforschung;

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Lehrach,  Hans
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

/persons/resource/persons50396

Krobitsch,  Sylvia
Neurodegenerative Disorders (Sylvia Krobitsch), Independent Junior Research Groups (OWL), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Kähler, C., Isensee, J., Nonhoff, U., Terrey, M., Hucho, T., Lehrach, H., et al. (2012). Ataxin-2-like is a regulator of stress granules and processing bodies. PLoS One, 7(11), e50134-e50134. doi:10.1371/journal.pone.0050134.


Cite as: https://hdl.handle.net/11858/00-001M-0000-000E-EC72-E
Abstract
Paralogs for several proteins implicated in neurodegenerative disorders have been identified and explored to further facilitate the identification of molecular mechanisms contributing to disease pathogenesis. For the disease-causing protein in spinocerebellar ataxia type 2, ataxin-2, a paralog of unknown function, termed ataxin-2-like, has been described. We discovered that ataxin-2-like associates with known interaction partners of ataxin-2, the RNA helicase DDX6 and the poly(A)-binding protein, and with ataxin-2 itself. Furthermore, we found that ataxin-2-like is a component of stress granules. Interestingly, sole ataxin-2-like overexpression led to the induction of stress granules, while a reduction of stress granules was detected in case of a low ataxin-2-like level. Finally, we observed that overexpression of ataxin-2-like as well as its reduction has an impact on the presence of microscopically visible processing bodies. Thus, our results imply a functional overlap between ataxin-2-like and ataxin-2, and further indicate a role for ataxin-2-like in the regulation of stress granules and processing bodies.