The HDAC Inhibitor SAHA Rescues the Skin Phenotype of CSB-deficient Mice (IMAGE)

Leibniz Institute for Environmental Medicine

The HDAC Inhibitor SAHA Rescues the Skin Phenotype of CSB-deficient Mice

Caption

Cockayne syndrome B (CSB) protein is known to be abundant in the nucleus where it participates in DNA repair. However, a fraction of CSB is located at the centrosome, the microtubule-organizing center of the cell, where it colocalizes with the alpha-tubulin acetyltransferase MEC-17 and the histone deacetylase HDAC6. The functional interplay between these proteins appears to be important for induction of acetyl-alpha-tubulin, a post-translational modification required for promoting the stress-protective mechanism autophagy. In the skin, CSB-induced autophagy protects integrity of the subcutaneous fat. Absence of a functional CSB protein in Cockayne syndrome leading to dysfunction of alpha-tubulin acetylation and autophagy as well as degeneration of subcutaneous fat in the skin of CSB-deficient mice can be prevented by administration of the pan-HDAC inhibitor SAHA indicating that CSB-mediated protein acetylation is critical for maintaining integrity of subcutaneous fat.

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IUF Leibniz Research Institute for Environmental Medicine

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