The Role of Diglycosyl Lipids in Photosynthesis and Membrane Lipid Homeostasis in Arabidopsis

ABSTRACTLipids exert diverse functions in living organisms. They form cellular membranes, store and transport energy and play signalling roles. Some lipid species function in all of these processes, making them ideal candidates to coordinate metabolism with cellular homeostasis and animal development. This theme was central to Suzanne Eaton's research in the fruit fly, Drosophila. Here, we discuss her work on membrane lipid homeostasis in changing environments and on functions for lipids in the Hedgehog signalling pathway. We further highlight lipoproteins as inter-organ carriers of lipids and lipid-linked morphogens, which communicate dietary and developmental signals throughout the organism.

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The yeast FIT2 homologs are necessary to maintain cellular proteostasis and membrane lipid homeostasis

Journal of Cell Science ◽

10.1242/jcs.248526 ◽

2020 ◽

Vol 133 (21) ◽

pp. jcs248526 ◽

Cited By ~ 1

Author(s):

Wei Sheng Yap ◽

Peter Shyu ◽

Maria Laura Gaspar ◽

Stephen A. Jesch ◽

Charlie Marvalim ◽

...

Keyword(s):

Saccharomyces Cerevisiae ◽

Endoplasmic Reticulum ◽

Lipid Droplets ◽

Membrane Lipid ◽

Model System ◽

Lipid Homeostasis ◽

Compensatory Mechanism ◽

Unfolded Protein ◽

Protein Response

ABSTRACTLipid droplets (LDs) are implicated in conditions of lipid and protein dysregulation. The fat storage-inducing transmembrane (FIT; also known as FITM) family induces LD formation. Here, we establish a model system to study the role of the Saccharomyces cerevisiae FIT homologues (ScFIT), SCS3 and YFT2, in the proteostasis and stress response pathways. While LD biogenesis and basal endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) remain unaltered in ScFIT mutants, SCS3 was found to be essential for proper stress-induced UPR activation and for viability in the absence of the sole yeast UPR transducer IRE1. Owing to not having a functional UPR, cells with mutated SCS3 exhibited an accumulation of triacylglycerol within the ER along with aberrant LD morphology, suggesting that there is a UPR-dependent compensatory mechanism that acts to mitigate lack of SCS3. Additionally, SCS3 was necessary to maintain phospholipid homeostasis. Strikingly, global protein ubiquitylation and the turnover of both ER and cytoplasmic misfolded proteins is impaired in ScFITΔ cells, while a screen for interacting partners of Scs3 identifies components of the proteostatic machinery as putative targets. Together, our data support a model where ScFITs play an important role in lipid metabolism and proteostasis beyond their defined roles in LD biogenesis.This article has an associated First Person interview with the first author of the paper.

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Participation of ABCA1 transporter in development of chronic obstructive pulmonary disease

I P Pavlov Russian Medical Biological Herald ◽

10.23888/pavlovj2020283360-370 ◽

2020 ◽

Vol 28 (3) ◽

pp. 360-370

Author(s):

Stanislav N. Kotlyarov ◽

Anna A. Kotlyarova

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Pulmonary Disease ◽

Significant Contribution ◽

Modern Medicine ◽

Lipid Homeostasis ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Reverse Transport ◽

Current Paradigm

Despite all achievements of the modern medicine, the problem of chronic obstructive pulmonary disease (COPD) does not lose its relevance. The current paradigm suggests a key role of macrophages in inflammation in COPD. Macrophages are known to be heterogeneous in their functions. This heterogeneity is determined by their immunometabolic profile and also by peculiarities of lipid homeostasis of cells. Aim. To analyze the role of the ABCA1 transporter, a member of the ABC A subfamily, in the pathogenesis of COPD. The expression of ABCA1 in lung tissues is on the second place after the liver, which shows the important role of the carrier and of lipid homeostasis in the function of lungs. Analysis of the literature shows that participation of the transporter in inflammation consists in regulation of the content of cholesterol in the lipid rafts of the membranes, in phagocytosis and apoptosis. Conclusion. Through regulation of the process of reverse transport of cholesterol in macrophages of lungs, ABCA1 can change their inflammatory response, which makes a significant contribution to the pathogenesis of COPD.

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Faculty Opinions recommendation of Structural basis for the transcriptional regulation of membrane lipid homeostasis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.4916990.4847096 ◽

2010 ◽

Author(s):

Roy Lancaster ◽

Florian Müller

Keyword(s):

Transcriptional Regulation ◽

Membrane Lipid ◽

Lipid Homeostasis ◽

Structural Basis

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High Fat Activates O-GlcNAcylation and Affects AMPK/ACC Pathway to Regulate Lipid Metabolism

Nutrients ◽

10.3390/nu13061740 ◽

2021 ◽

Vol 13 (6) ◽

pp. 1740

Author(s):

Yuning Pang ◽

Xiang Xu ◽

Xiaojun Xiang ◽

Yongnan Li ◽

Zengqi Zhao ◽

...

Keyword(s):

Lipid Metabolism ◽

High Fat Diet ◽

Lipid Synthesis ◽

Fat Deposition ◽

Liver Fat ◽

Lipid Homeostasis ◽

High Fat ◽

Dual Inhibitor ◽

Regulate Lipid Metabolism

A high-fat diet often leads to excessive fat deposition and adversely affects the organism. However, the mechanism of liver fat deposition induced by high fat is still unclear. Therefore, this study aimed at acetyl-CoA carboxylase (ACC) to explore the mechanism of excessive liver deposition induced by high fat. In the present study, the ORF of ACC1 and ACC2 were cloned and characterized. Meanwhile, the mRNA and protein of ACC1 and ACC2 were increased in liver fed with a high-fat diet (HFD) or in hepatocytes incubated with oleic acid (OA). The phosphorylation of ACC was also decreased in hepatocytes incubated with OA. Moreover, AICAR dramatically improved the phosphorylation of ACC, and OA significantly inhibited the phosphorylation of the AMPK/ACC pathway. Further experiments showed that OA increased global O-GlcNAcylation and agonist of O-GlcNAcylation significantly inhibited the phosphorylation of AMPK and ACC. Importantly, the disorder of lipid metabolism caused by HFD or OA could be rescued by treating CP-640186, the dual inhibitor of ACC1 and ACC2. These observations suggested that high fat may activate O-GlcNAcylation and affect the AMPK/ACC pathway to regulate lipid synthesis, and also emphasized the importance of the role of ACC in lipid homeostasis.

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Lipid Acyl Chain Remodeling in Yeast

Lipid Insights ◽

10.4137/lpi.s31780 ◽

2015 ◽

Vol 8s1 ◽

pp. LPI.S31780 ◽

Cited By ~ 1

Author(s):

Mike F. Renne ◽

Xue Bao ◽

Cedric H. De Smet ◽

Anton I. P. M. De Kroon

Keyword(s):

Intracellular Transport ◽

De Novo ◽

Acyl Chain ◽

Model Organism ◽

Lipid Synthesis ◽

Membrane Lipid ◽

Lipid Homeostasis ◽

Synthetic Process ◽

Acyl Chains ◽

Phospholipid Acyl Chain

Membrane lipid homeostasis is maintained by de novo synthesis, intracellular transport, remodeling, and degradation of lipid molecules. Glycerophospholipids, the most abundant structural component of eukaryotic membranes, are subject to acyl chain remodeling, which is defined as the post-synthetic process in which one or both acyl chains are exchanged. Here, we review studies addressing acyl chain remodeling of membrane glycerophospholipids in Saccharomyces cerevisiae, a model organism that has been successfully used to investigate lipid synthesis and its regulation. Experimental evidence for the occurrence of phospholipid acyl chain exchange in cardiolipin, phosphatidylcholine, phosphatidylinositol, and phosphatidylethanolamine is summarized, including methods and tools that have been used for detecting remodeling. Progress in the identification of the enzymes involved is reported, and putative functions of acyl chain remodeling in yeast are discussed.

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Dietary Selenium or Zinc Supplementation Restores Brain Lipid Composition and Membrane Fluidity in Protein-Undernourished Rats

Developmental Neuroscience ◽

10.1159/000462971 ◽

2016 ◽

Vol 38 (6) ◽

pp. 397-406

Author(s):

Olusegun L. Adebayo ◽

Bamidele A. Salau ◽

Rajat Sandhir ◽

Gbenga A. Adenuga

Keyword(s):

Membrane Fluidity ◽

Lipid Composition ◽

Zinc Supplementation ◽

Protective Role ◽

Membrane Lipid ◽

Limited Information ◽

Total Lipids ◽

Major Focus ◽

Membrane Lipid Composition

Studies have shown that protein undernutrition (PU) modifies the membrane lipid composition in the intestine and liver, as well as in plasma and other areas. However, there is limited information on the effect of PU on synaptosomal membrane lipid composition and fluidity and the protective role of selenium (Se) and zinc (Zn), which is a major focus of the present study. For 10 weeks, rats were fed diets containing 16% casein, which constituted the adequate protein diet, or 5% casein, representing the PU diet. The animals were supplemented with Se and Zn at a concentration of 0.15 and 227 mg L-1, respectively, in drinking water for 3 weeks. The results showed a significant increase in total lipids, glycolipids, triglycerides, cholesterol, and the cholesterol/phospholipid (Chol/PL) ratio, and a significant reduction in phospholipids and membrane fluidity. Se and Zn supplementation to PU rats, however, significantly lowered total lipids, glycolipids, triglycerides, cholesterol, and the Chol/PL ratio, while phospholipids and membrane fluidity were significantly restored. It is concluded that a perturbed lipid composition induced by PU affects the membrane structure and fluidity, which in turn influences membrane functions. The study suggests that Se and Zn supplementation might be beneficial in restoring the lipid dyshomeostasis associated with PU.

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