Dataset Information

Interplay Between Lipid Metabolism and Autophagy.

ABSTRACT: Autophagy is a self-eating process of using lysosomes to degrade macromolecular substances (e.g., proteins and organelles) that are damaged, degenerated, or aging. Lipid metabolism is the synthesis and degradation of lipids (e.g., triglycerides, steroids, and phospholipids) to generate energy or produce the structural components of cell membranes. There is a complex interplay between lipid metabolism (e.g., digestion, absorption, catabolism, biosynthesis, and peroxidation) and autophagy machinery, leading to the modulation of cell homeostasis, including cell survival and death. In particular, lipid metabolism is involved in the formation of autophagic membrane structures (e.g., phagophores and autophagosomes) during stress. Moreover, autophagy, especially selective autophagy (e.g., lipophagy, ferritinophagy, clockophagy, and mitophagy), promotes lipid catabolism or lipid peroxidation-induced ferroptosis through the degradation of various substances within the cell. A better understanding of the mechanisms of autophagy and possible links to lipid metabolism will undoubtedly promote potential treatments for a variety of diseases.

SUBMITTER: Xie Y

PROVIDER: S-EPMC7283384 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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Publications

Interplay Between Lipid Metabolism and Autophagy.

Xie Yangchun Y Li Jingbo J Kang Rui R Tang Daolin D

Frontiers in cell and developmental biology 20200603

Autophagy is a self-eating process of using lysosomes to degrade macromolecular substances (e.g., proteins and organelles) that are damaged, degenerated, or aging. Lipid metabolism is the synthesis and degradation of lipids (e.g., triglycerides, steroids, and phospholipids) to generate energy or produce the structural components of cell membranes. There is a complex interplay between lipid metabolism (e.g., digestion, absorption, catabolism, biosynthesis, and peroxidation) and autophagy machiner ...[more]

PMID: 32582708

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Project description:Due to the critical role played by autophagy in pathogen clearance, pathogens have developed diverse strategies to subvert it. Despite previous key findings of bacteria-autophagy interplay, asystems-level insight into selective targeting by the host and autophagy modulation by the pathogens is lacking. We predicted potential interactions between human autophagy proteins and effector proteins from 56 pathogenic bacterial species by identifying bacterial proteins predicted to have recognition motifs for selective autophagy receptors SQSTM1/p62, CALCOCO2/NDP52 and MAP1LC3/LC3. Using structure-based interaction prediction, we identified bacterial proteins capable to modify core autophagy components. Our analysis revealed that autophagy receptors in general potentially target mostly genus-specific proteins, and not those present in multiple genera. The complementarity between the predicted SQSTM1/p62 and CALCOCO2/NDP52 targets, which has been shown for Salmonella, Listeria and Shigella, could be observed across other pathogens. This complementarity potentially leaves the host more susceptible to chronic infections upon the mutation of autophagy receptors. Proteins derived from enterotoxigenic and non-toxigenic Bacillus outer membrane vesicles indicated that autophagy targets pathogenic proteins rather than non-pathogenic ones. We also observed apathogen-specific pattern as to which autophagy phase could be modulated by specific genera. We found intriguing examples of bacterial proteins that could modulate autophagy, and in turn being targeted by autophagy as ahost defense mechanism. We confirmed experimentally an interplay between a Salmonella protease, YhjJ and autophagy. Our comparative meta-analysis points out key commonalities and differences in how pathogens could affect autophagy and how autophagy potentially recognizes these pathogenic effectors. Abbreviations: ATG5: autophagy related 5; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; GST: glutathione S-transferase; LIR: MAP1LC3/LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3 alpha; OMV: outer membrane vesicles; SQSTM1/p62: sequestosome 1; SCV: Salmonella containing vesicle; TECPR1: tectonin beta-propeller repeat containing 1; YhjJ: hypothetical zinc-protease.

Dataset Information

Interplay Between Lipid Metabolism and Autophagy.

Publications

Interplay Between Lipid Metabolism and Autophagy.

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