
Autophagy is a highly conserved degradative process that removes damaged or unnecessary proteins and organelles, and recycles cytoplasmic contents during starvation. Autophagy is essential in physiological processes such as embryonic development but how autophagy is regulated by canonical developmental pathways is unclear. Here we show that the Hedgehog signalling pathway inhibits autophagosome synthesis, both in basal and in autophagy-induced conditions. This mechanism is conserved in mammalian cells and in Drosophila, and requires the orthologous transcription factors Gli2 and Ci, respectively. Furthermore, we identify that activation of the Hedgehog pathway reduces PERK levels, concomitant with a decrease in phosphorylation of the translation initiation factor eukaryotic initiation factor 2α, suggesting a novel target of this pathway and providing a possible link between Hedgehog signalling and autophagy.
Patched Receptors, 570, Transcription, Genetic, Fat Body, Kruppel-Like Transcription Factors, Down-Regulation, Receptors, Cell Surface, Zinc Finger Protein Gli2, Article, Receptors, G-Protein-Coupled, Mice, eIF-2 Kinase, Drosophila melanogaster, Gene Knockdown Techniques, Phagosomes, Autophagy, Animals, Drosophila Proteins, Humans, Hedgehog Proteins, HeLa Cells, Signal Transduction
Patched Receptors, 570, Transcription, Genetic, Fat Body, Kruppel-Like Transcription Factors, Down-Regulation, Receptors, Cell Surface, Zinc Finger Protein Gli2, Article, Receptors, G-Protein-Coupled, Mice, eIF-2 Kinase, Drosophila melanogaster, Gene Knockdown Techniques, Phagosomes, Autophagy, Animals, Drosophila Proteins, Humans, Hedgehog Proteins, HeLa Cells, Signal Transduction
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| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
