Metabolic disorders such as obesity and nonalcoholic fatty liver disease (NAFLD) are emerging disorders that affect the global population. One facet of the disorders is attributed to the disturbance of membrane lipid homeostasis. Perturbation of endoplasmic reticulum (ER) homeostasis through changes in membrane phospholipid composition results in activation of the unfolded protein response (UPR) and causes dramatic translational and transcriptional changes in cell. To restore cellular homeostasis, the three highly conserved UPR transducers ATF6, IRE1, and PERK mediate cellular processes upon ER stress. The roles of the UPR in proteostatic stress caused by the accumulation of misfolded protein is well understood but lipid perturbation-induced UPR remains elusive. We found that genetically attenuated PC synthesis in C. elegans causes lipid droplets accumulation if not for the intervention of the UPR program. Transcriptional profiling of lipid perturbation-induced ER stress animals shows a unique subset of genes modulated in an UPR-dependent manner that are unaffected by proteostatic stress. Among these, we identified IRE1-modulated autophagy genes that trigger liberation of free fatty acids from excess lipid droplets suggesting a stress release mechanism by which free fatty acids are rechannelling to restore lipid homeostasis. Considering the important role of lipid homeostasis and how its impairment contributes to the pathologies in metabolic diseases, our data uncovers the indispensable role of a fully functional UPR program in regulating lipid homeostais in the face of chronic ER stress.
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Specimen part
View SamplesWe used the microarray data to analyze host cells response on A549 cells infected with A/duck/Malaysia/F118/08/2004(H5N2)
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
View SamplesWe used the microarray data to analyze host cells response on A549 cells infected with A/Duck/Malaysia/01 (H9N2)
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
View SamplesWe used the microarray data to analyze host cells response on A549 cells infected with Influenza A virus (A/Singapore/478/2009 (pH1N1))
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
View SamplesWe used the microarray data to analyze host cells response on CEF cells infected with A/duck/Malaysia/F118/08/2004(H5N2)
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
View SamplesWe used the microarray data to analyze host cells response on CEF cells infected with A/Duck/Malaysia/01 (H9N2)
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
View SamplesWe used the microarray data to analyse the host cell responses on mouse macrophages infected with the three Influenza A viruses
Systems-based approach to examine the cytokine responses in primary mouse lung macrophages infected with low pathogenic avian Influenza virus circulating in South East Asia.
Specimen part
View SamplesWe used the microarray data to analyze host cells response on Hep2 cells infected with HRSV.
No associated publication
Specimen part, Time
View SamplesWe used the microarray data to analyze host cells response on CEF cells infected with A/WSN/33 (H1N1)
Activation of type I and III interferon signalling pathways occurs in lung epithelial cells infected with low pathogenic avian influenza viruses.
Specimen part, Cell line, Time
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