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  4. Neural Regulation of Mitochondrial Stress Response in Caenorhabditis elegans
 
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Neural Regulation of Mitochondrial Stress Response in Caenorhabditis elegans

Date Issued
2016
Date
2016
Author(s)
Lin, Chih-Ta
DOI
10.6342/NTU201602858
URI
http://ntur.lib.ntu.edu.tw//handle/246246/271720
Abstract
Compartment-specific stress responses, including cytosolic heat shock response (HSR), the endoplasmic reticulum unfolded protein response (UPRER), and the mitochondrial unfolded protein response (UPRmt), protect animals against proteotoxic stress. Age-dependent decline in cellular functions and organismal physiology is associated with dysregulated protein homeostasis and mitochondrial function. Systemic proteostasis in the nematode Caenorhabditis elegans could be regulated by mitochondrial respiration in the neurons, but the molecular mechanisms of such intercellular control of protein homeostasis remains unclear. Here we report that the C. elegans mitochondrial fusion protein FZO-1/Mitofusin controlled UPRmt in a cell non-autonomous manner. Mutations of fzo-1 caused pleiotropic phenotypes, including slow development, reduced fecundity, accelerated neuronal aging, and maladapted UPRmt. Neuronal mitochondrial defects and aging signs of the neurites were rescued by neuron-autonomous FZO-1 functions. The maladapted UPRmt in the intestine was moderately rescued by intestinal FZO-1 expression. Unexpectedly, aberrant intestinal UPRmt of the fzo-1 mutants was significantly ameliorated by neuronal FZO-1. Neuronal FZO-1 also partially rescued the slow development of the fzo-1 mutant. We are now exploring neuron-derived signals that potentially mediate such non-autonomous effects on systemic mitochondrial proteostasis. Progress in this proposal could further our understanding of how mitochondria-mediated, neuron-derived signals control systemic protein homeostasis and cellular aging at the organismal level.
Subjects
C. elegans
Mitochondria
FZO-1/Mitofusin
Unfolded protein response
Neuronal signal
Type
thesis
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