Hedgehog signalling regulates autophagy
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Access through your institution Buy or subscribe Autophagy, a degradative pathway for removal of cytoplasmic proteins and organelles through sequestration in autophagosomes and lysosomal
degradation, has been suggested to be important for embryonic development. Rubinsztein and colleagues report in _Nature Communications_ (http://doi.org/jrd) that autophagy can be controlled
by the Hedgehog (HH) signalling pathway in mammalian cells and in _Drosophila melanogaster_. Activation of HH signalling by a variety of means impairs autophagy; specifically, autophagosome
formation. Known components of the HH signalling pathway — the receptors PTCH1 and PTCH2, the transmembrane protein SMO (which acts downstream of the receptors) and the transcription factor
GLI2 in mammalian cells — are also required for HH effects on autophagy. Regulation of autophagy by the HH pathway was also conserved in _Drosophila_. In an effort to identify downstream
targets of HH signalling that may directly modulate autophagy, the authors assessed changes in the expression patterns of an array of autophagy genes in response to HH signalling activation.
They found that PERK (also known as EIF2AK3) and GABARAP1, both implicated in autophagy, were reduced following HH activation; however, additional effectors were also likely to be
implicated in autophagy regulation by the HH pathway. The mechanistic details of how the HH pathway controls autophagy await future study. This is a preview of subscription content, access
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Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support Authors * Sowmya Swaminathan View author publications You can also search for this author inPubMed
Google Scholar RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Swaminathan, S. Hedgehog signalling regulates autophagy. _Nat Cell Biol_ 14, 1250 (2012).
https://doi.org/10.1038/ncb2650 Download citation * Published: 30 November 2012 * Issue Date: December 2012 * DOI: https://doi.org/10.1038/ncb2650 SHARE THIS ARTICLE Anyone you share the
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