ArticleCell death & disease2014
The PERK pathway independently triggers apoptosis and a Rac1/Slpr/JNK/Dilp8 signaling favoring tissue homeostasis in a chronic ER stress Drosophila model.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
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- A statistical mechanics investigation of unfolded protein response across organisms.Scientific reports · 2024Article
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- Collective cell migration relies on PPP1R15-mediated regulation of the endoplasmic reticulum stress response.Current biology : CB · 2024Article
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- Characterisation of the in-vivo miRNA landscape in Drosophila ribonuclease mutants reveals Pacman-mediated regulation of the highly conserved let-7 cluster during apoptotic processes.Frontiers in genetics · 2024Article
- Slik maintains tissue homeostasis by preventing JNK-mediated apoptosis.Cell division · 2023Article
- Nacα protects the larval fat body from cell death by maintaining cellular proteostasis in Drosophila.Nature communications · 2023Article
- The small compound Icerguastat reduces muscle defects in oculopharyngeal muscular dystrophy through the PERK pathway of the unfolded protein response.Open biology · 2023Article
- Mitochondrial remodelling is essential for female germ cell differentiation and survival.PLoS genetics · 2023Article
- Chitooligosaccharide prevents vascular endothelial cell apoptosis by attenuation of endoplasmic reticulum stress via suppression of oxidative stress through Nrf2-SOD1 up-regulation.Pharmaceutical biology · 2022Article
- Shrimp Lipid Prevents Endoplasmic Reticulum-Mediated Endothelial Cell Damage.Foods (Basel, Switzerland) · 2022Article
- A genome-wide CRISPR screen identifies DPM1 as a modifier of DPAGT1 deficiency and ER stress.PLoS genetics · 2022Article
- Drosophila Unfolded Protein Response (UPR) Assays In Vitro and In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The steroid-hormone ecdysone coordinates parallel pupariation neuromotor and morphogenetic subprograms via epidermis-to-neuron Dilp8-Lgr3 signal induction.Nature communications · 2021Article
- Signaling Nodes Associated with Endoplasmic Reticulum Stress during NAFLD Progression.Biomolecules · 2021Review
- Chinese Herbal Medicine Alleviates Myocardial Ischemia/Reperfusion Injury by Regulating Endoplasmic Reticulum Stress.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Epithelial cell-turnover ensures robust coordination of tissue growth in Drosophila ribosomal protein mutants.PLoS genetics · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The endoplasmic reticulum (ER) has a major role in protein folding. The accumulation of unfolded proteins in the ER induces a stress, which can be resolved by the unfolded protein response (UPR). Chronicity of ER stress leads to UPR-induced apoptosis and in turn to an unbalance of tissue homeostasis. Although ER stress-dependent apoptosis is observed in a great number of devastating human diseases, how cells activate apoptosis and promote tissue homeostasis after chronic ER stress remains poorly understood. Here, using the Drosophila wing imaginal disc as a model system, we validated that Presenilin overexpression induces chronic ER stress in vivo. We observed, in this novel model of chronic ER-stress, a PERK/ATF4-dependent apoptosis requiring downregulation of the antiapoptotic diap1 gene. PERK/ATF4 also activated the JNK pathway through Rac1 and Slpr activation in apoptotic cells, leading to the expression of Dilp8. This insulin-like peptide caused a developmental delay, which partially allowed the replacement of apoptotic cells. Thanks to a novel chronic ER stress model, these results establish a new pathway that both participates in tissue homeostasis and triggers apoptosis through an original regulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.