Ral GTPase and the exocyst regulate autophagy in a tissue‐specific manner
Open accessAbstract
Autophagy traffics cellular components to the lysosome for degradation. Ral GTPase and the exocyst have been implicated in the regulation of stress-induced autophagy, but it is unclear whether they are global regulators of this process. Here, we investigate Ral function in different cellular contexts in Drosophila and find that it is required for autophagy during developmentally regulated cell death in salivary glands, but does not affect starvation-induced autophagy in the fat body. Furthermore, knockdown of exocyst subunits has a similar effect, preventing autophagy in dying cells but not in cells of starved animals. Notch activity is elevated in dying salivary glands, this change in Notch signaling is influenced by Ral, and decreased Notch function influences autophagy. These data indicate that Ral and the exocyst regulate autophagy in a context-dependent manner, and that in dying salivary glands, Ral mediates autophagy, at least in part, by regulation of Notch.
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Developmental degradation of Drosophila salivary glands by autophagy requires Utx, miR-14, Rala, Drpr, and Mcr.
“Moreover, the developmental degradation of Drosophila salivary glands by autophagy requires the activity of: (1) Utx histone demethylase (Utx), which contributes to the transcriptional regulation of apoptosis and autophagy genes [839]; (2) miR-14, which specifically activates autophagy-dependent cell death by modulating multiple IP3-driven signaling pathways upon targeting inositol 1,4,5-triphosph”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [841]
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The exocyst complex controls multiple events in the pathway of regulated exocytosisPreprint
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- Authors
- Tracy, K., Velentzas, P. D., & Baehrecke, E. H.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Baehrecke, Eric H
- Venue
- The EMBO Reports
- Published
- 2015-11-23
- Volume
- 17
- Issue
- 1
- Pages
- 110-121
- ISSN
- 1469-221X (ISSN-L)
- 1469-3178
- PMC
- PMC4718410
- OpenAlex
- W2172881016
- Cited by
- 22
- References
- 45
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 3 · 2020: 1 · 2019: 1 · 2018: 6 · 2017: 4 · 2015: 1
- FWCI
- 2.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- EMBO Reports (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship@UMassChan (submittedVersion)
- Funders
- NIH (GM079431)
- Ellison Medical Foundation Scholar
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- Ral GTPase, exocyst, autophagy, Notch signaling, salivary glands, developmental cell death, starvation-induced autophagy, fat body, lysosomal degradation, tissue-specific gene regulation, Drosophila
- MeSH terms
- Animals, Autophagy, Drosophila melanogaster, Fat Body, Gene Expression Regulation, Salivary Glands, Starvation, Stress, Physiological, Cell Death, ral GTP-Binding Proteins, Drosophila Proteins, Receptors, Notch
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