Journal
CELL REPORTS
Volume 24, Issue 6, Pages 1407-1414Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.07.023
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Funding
- SNSF [31003A_127308]
- Novartis Foundation for Medical-Biological Research
- Desiree and Nils Yde Foundation [420-14]
- Bangerter-Rhyner Foundation [8472/HEG-DSV]
- Nora van Meeuwen-Haefliger Foundation
- Mach-Gaensslen Foundation
- Forschungsfonds of Basel University
- ERC (grant UPR Neuro) [282280]
- MRC
- Alzheimer's Society
- ARUK/DRI
- Telethon Italy [GGP12162, GPP10005]
- AIRC Italy [IG15748]
- ERC ERMITO, FP7 CIG CristOpa [PCIG13-GA-2013-618697]
- MIUR FIRB Automed [RBAP-11Z3YA_005]
- European Research Council (ERC) [282280] Funding Source: European Research Council (ERC)
- Swiss National Science Foundation (SNF) [31003A_127308] Funding Source: Swiss National Science Foundation (SNF)
- MRC [MC_U132692719, UKDRI-2001] Funding Source: UKRI
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Stress adaptation is essential for neuronal health. While the fundamental role of mitochondria in neuronal development has been demonstrated, it is still not clear how adult neurons respond to alterations in mitochondrial function and how neurons sense, signal, and respond to dysfunction of mitochondria and their interacting organelles. Here, we show that neuron-specific, inducible in vivo ablation of the mitochondrial fission protein Drp1 causes ER stress, resulting in activation of the integrated stress response to culminate in neuronal expression of the cytokine Fgf21. Neuron-derived Fgf21 induction occurs also in murine models of tauopathy and prion disease, highlighting the potential of this cytokine as an early biomarker for latent neurodegenerative conditions.
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