Genomics

Dataset Information

0

Lipid biosynthesis coordinates a Mitochondrial to Cytosolic Stress Response


ABSTRACT: Defects in mitochondrial metabolism have been increasingly linked with age-onset protein misfolding diseases such as Alzheimer’s, Parkinson’s, and Huntington’s. In response to protein folding stress, compartment-specific unfolded protein responses (UPRs) within the endoplasmic reticulum, mitochondria, and cytosol work in parallel to ensure cellular protein homeostasis. While perturbation of individual compartments can make other compartments more susceptible to protein stress, the cellular conditions that trigger cross-communication between the individual UPRs remain poorly understood. We have uncovered a conserved, robust mechanism linking mitochondrial protein homeostasis and the cytosolic folding environment through changes in lipid homeostasis. Metabolic restructuring caused by mitochondrial stress or small molecule activators trigger changes in gene expression coordinated uniquely by both the mitochondrial and cytosolic UPRs, protecting the cell from disease-associated proteins. Our data suggest an intricate and unique system of communication between UPRs in response to metabolic changes that could unveil new targets for diseases of protein misfolding.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE83722 | GEO | 2016/09/08

SECONDARY ACCESSION(S): PRJNA326871

REPOSITORIES: GEO

Similar Datasets

2016-09-08 | E-GEOD-83722 | biostudies-arrayexpress
2016-06-28 | E-GEOD-75247 | biostudies-arrayexpress
2016-06-28 | E-GEOD-75410 | biostudies-arrayexpress
2016-06-28 | GSE75410 | GEO
2016-06-28 | GSE75247 | GEO
2022-10-04 | GSE198540 | GEO
2019-01-12 | GSE116749 | GEO
2019-03-13 | PXD012867 | Pride
2024-04-17 | GSE246899 | GEO
2021-07-26 | GSE146458 | GEO