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DYRK1B regulates Hedgehog-induced microtubule acetylation.
Rajeev Singh1, Philipp Simon Holz1, Katrin Roth2
1Institute of Molecular Biology and Tumor Research (IMT), Center for Tumor- and Immune Biology (ZTI), Philipps University, Hans-Meerwein-Str. 3, 35043, Marburg, Germany.
Cellular and Molecular Life Sciences : CMLS
|October 15, 2018
Summary
Hedgehog (Hh) signaling regulates microtubule (MT) acetylation by increasing DYRK1B kinase activity, which inhibits HDAC6. This leads to increased acetylated MTs, impacting cell migration and mitochondrial transport.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Posttranslational modifications (PTMs) of tubulin are crucial for microtubule (MT) cytoskeleton functions.
- Intercellular signaling's role in regulating MT-PTM-dependent processes is not well understood.
Purpose of the Study:
- To investigate how Hedgehog (Hh) signaling influences MT acetylation state in mammalian cells.
- To elucidate the molecular mechanisms linking Hh signaling to MT acetylation.
Main Methods:
- Analysis of Hh signaling pathway components and their effect on MT-associated kinases and deacetylases.
- Assessment of tubulin acetylation levels.
- Evaluation of MT-dependent cellular processes like mitochondrial transport and cell migration.
Main Results:
- Hh pathway activation elevates DYRK1B kinase levels.
- DYRK1B phosphorylates and inhibits GSK3β, subsequently suppressing HDAC6 activity.
- Inhibition of HDAC6, a major tubulin deacetylase, results in increased MT acetylation.
- Elevated MT acetylation facilitates MT-dependent processes, including mitochondrial transport, cell polarization, and migration.
Conclusions:
- Intercellular Hh signaling modulates the MT cytoskeleton by altering tubulin acetylation levels.
- This regulation impacts key MT-dependent cellular functions, highlighting a novel link between cell communication and cytoskeletal dynamics.
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