scholarly journals A salicylic acid derivative extends the lifespan of Caenorhabditis elegans by activating autophagy and the mitochondrial unfolded protein response

Aging Cell ◽  
2018 ◽  
Vol 17 (6) ◽  
pp. e12830 ◽  
Author(s):  
Mehrnaz Shamalnasab ◽  
Simon-Pierre Gravel ◽  
Julie St-Pierre ◽  
Lionel Breton ◽  
Sibylle Jäger ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Caenorhabditis Elegans ◽  
Unfolded Protein Response ◽  
Acid Derivative ◽  
Unfolded Protein ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

scholarly journals Activation of the mitochondrial unfolded protein response does not predict longevity in Caenorhabditis elegans

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Christopher F. Bennett ◽  
Helen Vander Wende ◽  
Marissa Simko ◽  
Shannon Klum ◽  
Sarah Barfield ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Unfolded Protein Response ◽  
Unfolded Protein ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

scholarly journals The Mitochondrial Unfolded Protein Response Protects against Anoxia in Caenorhabditis elegans

PLoS ONE ◽  
2016 ◽  
Vol 11 (7) ◽  
pp. e0159989 ◽  
Author(s):  
Salvador Peña ◽  
Teresa Sherman ◽  
Paul S. Brookes ◽  
Keith Nehrke
Keyword(s):  
Caenorhabditis Elegans ◽  
Unfolded Protein Response ◽  
Unfolded Protein ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

scholarly journals FSHR-1/GPCR Regulates the Mitochondrial Unfolded Protein Response in Caenorhabditis elegans

Genetics ◽  
2019 ◽  
Vol 214 (2) ◽  
pp. 409-418 ◽  
Author(s):  
Sungjin Kim ◽  
Derek Sieburth
Keyword(s):  
Caenorhabditis Elegans ◽  
Unfolded Protein Response ◽  
Mitochondrial Stress ◽  
Unfolded Protein ◽  
Mitochondrial Homeostasis ◽  
Link Type ◽  
Link Functions ◽  
Evolutionarily Conserved ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

The mitochondrial unfolded protein response (UPRmt) is an evolutionarily conserved adaptive response that functions to maintain mitochondrial homeostasis following mitochondrial damage. In Caenorhabditis elegans, the nervous system plays a central role in responding to mitochondrial stress by releasing endocrine signals that act upon distal tissues to activate the UPRmt. The mechanisms by which mitochondrial stress is sensed by neurons and transmitted to distal tissues are not fully understood. Here, we identify a role for the conserved follicle-stimulating hormone G protein-coupled receptor, FSHR-1, in promoting UPRmt activation. Genetic deficiency of fshr-1 severely attenuates UPRmt activation and organism-wide survival in response to mitochondrial stress. FSHR-1 functions in a common genetic pathway with SPHK-1/sphingosine kinase to promote UPRmt activation, and FSHR-1 regulates the mitochondrial association of SPHK-1 in the intestine. Through tissue-specific rescue assays, we show that FSHR-1 functions in neurons to activate the UPRmt, to promote mitochondrial association of SPHK-1 in the intestine, and to promote organism-wide survival in response to mitochondrial stress. We propose that FSHR-1 functions cell nonautonomously in neurons to activate UPRmt upstream of SPHK-1 signaling in the intestine.

scholarly journals Mitochondrial Unfolded Protein Response to Microgravity Stress in Nematode Caenorhabditis elegans

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Peidang Liu ◽  
Dan Li ◽  
Wenjie Li ◽  
Dayong Wang
Keyword(s):  
Caenorhabditis Elegans ◽  
Unfolded Protein Response ◽  
Simulated Microgravity ◽  
Biological Effects ◽  
Molecular Response ◽  
Protective Response ◽  
Unfolded Protein ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

Abstract Caenorhabditis elegans is useful for assessing biological effects of spaceflight and simulated microgravity. The molecular response of organisms to simulated microgravity is still largely unclear. Mitochondrial unfolded protein response (mt UPR) mediates a protective response against toxicity from environmental exposure in nematodes. Using HSP-6 and HSP-60 as markers of mt UPR, we observed a significant activation of mt UPR in simulated microgravity exposed nematodes. The increase in HSP-6 and HSP-60 expression mediated a protective response against toxicity of simulated microgravity. In simulated microgravity treated nematodes, mitochondria-localized ATP-binding cassette protein HAF-1 and homeodomain-containing transcriptional factor DVE-1 regulated the mt UPR activation. In the intestine, a signaling cascade of HAF-1/DVE-1-HSP-6/60 was required for control of toxicity of simulated microgravity. Therefore, our data suggested the important role of mt UPR activation against the toxicity of simulated microgravity in organisms.

scholarly journals At the heart of mitochondrial quality control: many roads to the top

2021 ◽  
Author(s):  
Roberta A. Gottlieb ◽  
Honit Piplani ◽  
Jon Sin ◽  
Savannah Sawaged ◽  
Syed M. Hamid ◽  
...  
Keyword(s):  
Quality Control ◽  
Unfolded Protein Response ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Quality Control ◽  
Unfolded Protein ◽  
Selective Elimination ◽  
Protein Response ◽  
Mitochondrial Unfolded Protein Response

AbstractMitochondrial quality control depends upon selective elimination of damaged mitochondria, replacement by mitochondrial biogenesis, redistribution of mitochondrial components across the network by fusion, and segregation of damaged mitochondria by fission prior to mitophagy. In this review, we focus on mitochondrial dynamics (fusion/fission), mitophagy, and other mechanisms supporting mitochondrial quality control including maintenance of mtDNA and the mitochondrial unfolded protein response, particularly in the context of the heart.

Sign in / Sign up

Export Citation Format

Share Document