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Article Addendum
HDAC6 at the Intersection of Autophagy, the Ubiquitin-proteasome System, and Neurodegeneration
Udai Bhan Pandey, Yakup Batlevi, Eric H. Baehrecke and J. Paul Taylor
volume 3 | issue 6
November/December 2007Pages: 643 - 645
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The two major intracellular catabolic pathways, the ubiquitin-proteasome system (UPS) and macroautophagy (autophagy), have each been implicated as playing roles in neurodegenerative proteinopathies1, 2. We have investigated the relationship between the UPS and autophagy using Drosophila models of neurodegenerative diseases. We identified histone deacetylase 6 (HDAC6) as a genetic modifier of polyglutamine-induced neurodegeneration and determined that its mechanism of action is autophagy-dependent3. The ability of HDAC6 to suppress degeneration has been extended to additional neurodegenerative disease models, including a fly model expressing pathologic Aβ fragments presented here, but is not a universal modifier of degenerative phenotypes. Importantly, HDAC6 was also found to suppress degeneration associated with proteasome mutations in an autophagy-dependent manner, revealing a compensatory relationship between these two degradation pathways. Our findings indicate that HDAC6 facilitates degradation of potentially noxious protein substrates, contributing vitally to the neuroprotective role of autophagy.
Authors
Udai Bhan Pandey
University of Pennsylvania School of Medicine
Yakup Batlevi
University of Maryland Biotechnology Institute
Eric H. Baehrecke
University of Massachusetts Medical School
J. Paul Taylor
Department of Developmental Neurobiology; St. Jude Children’s Research Hospital; Memphis, TN USA
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.