Article
Biochemistry & Molecular Biology
Alessio Reggio, Viviana Buonomo, Rayene Berkane, Ramachandra M. Bhaskara, Mariana Tellechea, Ivana Peluso, Elena Polishchuk, Giorgia Di Lorenzo, Carmine Cirillo, Marianna Esposito, Adeela Hussain, Antje K. Huebner, Christian A. Hubner, Carmine Settembre, Gerhard Hummer, Paolo Grumati, Alexandra Stolz
Summary: The degradation of the endoplasmic reticulum via selective autophagy is crucial for cellular homeostasis. FAM134A and FAM134C have been identified as ER-phagy receptors that can induce ER fragmentation and lysosomal degradation. The FAM134 paralogues play a significant role in maintaining ER morphology and increasing ER-phagy flux.
Review
Biochemistry & Molecular Biology
Keisuke Mochida, Hitoshi Nakatogawa
Summary: Autophagy is a degradation system in eukaryotic cells that controls the mass and functions of organelles by degrading excess or defective portions. The endoplasmic reticulum (ER) is an organelle with specific functions that dynamically changes its mass and shape to maintain or regulate its functions. Elaborate mechanisms are required for the proper degradation of the ER.
Article
Agriculture, Dairy & Animal Science
Muhammad Rosyid Ridlo, Eui Hyun Kim, Eun Pyo Kim, Geon A. Kim
Summary: In this study, the application of miR-143 (mimics and inhibitors) to porcine parthenogenetically activated embryos showed that the miR-143 inhibitor can improve embryo development to the blastocyst stage, and is associated with increased activity of autophagy and ER-phagy as well as higher expression levels of genes related to embryo quality.
Article
Cell Biology
Natalia Jimenez-Moreno, Carla Salomo-Coll, Laura C. Murphy, Simon Wilkinson
Summary: Autophagy is an important cellular process for maintaining cellular homeostasis. However, current assays to measure autophagy flux are not ideal for providing accurate quantitative results. In this study, the researchers validate the use of a fluorescent probe, SRAI, for monitoring ER-phagy, a pathway involved in maintaining ER homeostasis. They also provide a detailed protocol for quantifying autophagic flux using automated microscopy and high throughput analysis. Overall, this probe offers a reliable and convenient tool for measuring ER-phagy.
Review
Cell Biology
Jiahui Li, Enfeng Gao, Chenguang Xu, Hongna Wang, Yongjie Wei
Summary: ER-phagy is a crucial mechanism for ER quality control, transporting damaged ER fragments to the lysosome for degradation to eliminate abnormal proteins and membrane lipids. Its deficiency can facilitate viral infection, highlighting its role in host defense against pathogens.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Lorenzo Picchianti, Victor Sanchez de Medina Hernandez, Ni Zhan, Nicholas A. T. Irwin, Roan Groh, Madlen Stephani, Harald Hornegger, Rebecca Beveridge, Justyna Sawa-Makarska, Thomas Lendl, Nenad Grujic, Christin Naumann, Sascha Martens, Thomas A. Richards, Tim Clausen, Silvia Ramundo, G. Elif Karagoz, Yasin Dagdas
Summary: UFMylation is a crucial covalent modification process that maintains endoplasmic reticulum homeostasis. Stalled translation triggers UFMylation of ER-bound ribosomes, activating C53-mediated autophagy for clearance of toxic polypeptides. The study reveals the ancestral role of sAIMs in UFMylation-dependent fine-tuning of C53-mediated autophagy activation, showing that C53 and sAIMs are conserved across eukaryotes but lost in fungi and certain algal lineages.
Review
Cell Biology
Wei Chen, Xueqian Ouyang, Linxi Chen, Lanfang Li
Summary: Selective autophagy is a process in which specific intracellular components are degraded through the activity of selective autophagy receptors. CALCOCO family proteins are newly identified receptors that play important roles in different selective autophagy pathways, including ER-phagy, Golgiphagy, mitophagy, and xenophagy. These proteins interact with ATG8/LC3 and ubiquitin to mediate cargo recruitment and degradation.
JOURNAL OF CELLULAR PHYSIOLOGY
(2022)
Article
Toxicology
Fujing Wei, Aimin Yang, Zhao Zhao, Huifang An, Yu Li, Yixiang Duan
Summary: This study explored the relationship between ER stress and ER-phagy induced by the emerging nanoparticles CdTe-QDs and revealed its molecular mechanism. The results showed that CdTe-QDs increased ROS accumulation and triggered ER stress, leading to the activation of autophagy and ER-phagy. Importantly, it was found that CdTe-QDs activated autophagy by up-regulating the transcription of core autophagy machinery, and the induced ER-phagy was mediated by Atg11/Atg40/Lst1-Sec23.
TOXICOLOGY LETTERS
(2022)
Review
Cell Biology
Ming Yang, Shilu Luo, Xi Wang, Chenrui Li, Jinfei Yang, Xuejing Zhu, Li Xiao, Lin Sun
Summary: The endoplasmic reticulum (ER) is crucial for maintaining cellular homeostasis, and ER-phagy, a selective form of autophagy, helps remove damaged ER to protect cells from harm caused by excessive ER stress. Many receptor-mediated ER-phagy pathways have been discovered in recent years, highlighting the importance of this newly identified autophagy process in maintaining cellular health.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Immunology
Shiping Liu, Xiaoyu Fang, Ruiyao Zhu, Jing Zhang, Huijuan Wang, Jiaxi Lei, Chaoqun Wang, Lu Wang, Liying Zhan
Summary: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are the main causes of morbidity and mortality in critically ill patients, and are typically treated with general supportive treatments. However, endoplasmic reticulum autophagy (ER-phagy) has been identified as a crucial process for maintaining cellular homeostasis and improving the internal environment. This review summarizes the definition, epidemiology, and pathophysiology of ALI/ARDS, as well as discusses the regulatory mechanisms and functions of ER-phagy in the context of immunity, inflammation, apoptosis, pathogen infection, and fibrosis. The potential role of ER-phagy in improving the prognosis of ALI/ARDS is also explored.
FRONTIERS IN IMMUNOLOGY
(2023)
Review
Neurosciences
Melissa A. Hill, Alex M. Sykes, George D. Mellick
Summary: There are various cellular mechanisms involved in neurodegenerative diseases, and the accumulation of unwanted cellular products with age is a common factor. Autophagy plays a significant role in maintaining neuronal homeostasis and disruption in autophagy can contribute to disease development. Recently, the role of ER-phagy in regulating ER morphology and response to cellular stress has been explored in relation to neurodegenerative diseases. This review discusses current research on ER-phagy and its involvement in these diseases.
JOURNAL OF NEUROSCIENCE RESEARCH
(2023)
Article
Cell Biology
Tomoyuki Fukuda, Tetsu Saigusa, Kentaro Furukawa, Keiichi Inoue, Shun-ichi Yamashita, Tomotake Kanki
Summary: The endoplasmic reticulum (ER) undergoes selective autophagy called reticulophagy or ER-phagy. Reticulon- and receptor expression enhancing protein (REEP)-like ER-shaping proteins, such as budding yeast Atg40, act as reticulophagy receptors to stabilize the phagophore on the ER by interacting with phagophore-conjugated Atg8. Hva22, a REEP family protein in fission yeast, promotes reticulophagy without Atg8-binding capacity and its role can be replaced by expressing Atg40 independently of its Atg8-binding ability.
Review
Physiology
Fulvio Reggiori, Maurizio Molinari
Summary: ER-phagy is the process of degrading portions of the endoplasmic reticulum (ER) within lysosomes or vacuoles. It plays a role in recycling cytoplasmic material and organelles, regulating ER size and activity, and removing potentially cytotoxic material. Dysfunctional ER-phagy is associated with specific human diseases and can be targeted by pathogens.
PHYSIOLOGICAL REVIEWS
(2022)
Review
Biochemistry & Molecular Biology
Debora Gentile, Marianna Esposito, Paolo Grumati
Summary: Autophagy is a cellular cleaning system that maintains metabolic balance and plays a crucial role in sustaining malignant cellular growth during tumorigenesis.
FRONTIERS IN MOLECULAR BIOSCIENCES
(2022)
Article
Biology
Maria Sol Herrera-Cruz, Megan C. Yap, Nasser Tahbaz, Keelie Phillips, Laurel Thomas, Gary Thomas, Thomas Simmen
Summary: Rab32 promotes degradation of mitochondrial-proximal ER membranes via autophagy with the help of its effector RTN3L, a process proposed to be termed MAM-phagy.
Article
Multidisciplinary Sciences
Juncal Garcia-Garcia, Katrine Stange Overa, Waqas Khan, Eva Sjottem
Summary: TRIM32 is regulated by post-translational modifications of three lysine residues and a conserved PEST sequence, with the PEST sequence directing cleavage of TRIM32 and lysine residues being involved in its auto-ubiquitylation activity. The short isoform of TRIM32 is catalytic inactive, possibly playing a dominant negative role in cellular processes.
Review
Cell Biology
Trond Lamark, Terje Johansen
Summary: Selective autophagy is the degradation of specific intracellular components via selective autophagy receptors, which interact with autophagy-related proteins and may or may not depend on ubiquitin labeling of the cargo.
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 37
(2021)
Editorial Material
Cell Biology
Yakubu Princely Abudu, Stephane Mouilleron, Sharon A. Tooze, Trond Lamark, Terje Johansen
Summary: Research has identified SAMM50 as a receptor for basal mitophagy, mediating the process through interaction with Atg8-family proteins and SQSTM1/p62. During a metabolic switch to oxidative phosphorylation, SAMM50 cooperates with SQSTM1 to facilitate efficient basal mitophagy.
Editorial Material
Cell Biology
Thaddaeus Mutugi Nthiga, Birendra Kumar Shrestha, Trond Lamark, Terje Johansen
Summary: Cellular stress response mechanisms can lead to an increase in organellar quantity and volume, which are cleared through autophagy. A recent study identified CALCOCO1 as a receptor for Golgiphagy in response to nutrient deprivation.
Review
Biochemistry & Molecular Biology
Daniel J. Klionsky, Giulia Petroni, Ravi K. Amaravadi, Eric H. Baehrecke, Andrea Ballabio, Patricia Boya, Jose Manuel Bravo-San Pedro, Ken Cadwell, Francesco Cecconi, Augustine M. K. Choi, Mary E. Choi, Charleen T. Chu, Patrice Codogno, Maria Isabel Colombo, Ana Maria Cuervo, Vojo Deretic, Ivan Dikic, Zvulun Elazar, Eeva-Liisa Eskelinen, Gian Maria Fimia, David A. Gewirtz, Douglas R. Green, Malene Hansen, Marja Jaattela, Terje Johansen, Gabor Juhasz, Vassiliki Karantza, Claudine Kraft, Guido Kroemer, Nicholas T. Ktistakis, Sharad Kumar, Carlos Lopez-Otin, Kay F. Macleod, Frank Madeo, Jennifer Martinez, Alicia Melendez, Noboru Mizushima, Christian Munz, Josef M. Penninger, Rushika M. Perera, Mauro Piacentini, Fulvio Reggiori, David C. Rubinsztein, Kevin M. Ryan, Junichi Sadoshima, Laura Santambrogio, Luca Scorrano, Hans-Uwe Simon, Anna Katharina Simon, Anne Simonsen, Alexandra Stolz, Nektarios Tavernarakis, Sharon A. Tooze, Tamotsu Yoshimori, Junying Yuan, Zhenyu Yue, Qing Zhong, Lorenzo Galluzzi, Federico Pietrocola
Summary: Autophagy is crucial for maintaining cellular and organismal homeostasis, and dysfunction in autophagy is implicated in the pathogenesis of major human disorders across various organ systems.
Article
Cell Biology
Yakubu Princely Abudu, Birendra Kumar Shrestha, Wenxin Zhang, Anthimi Palara, Hanne Britt Brenne, Kenneth Bowitz Larsen, Deanna Lynn Wolfson, Gianina Dumitriu, Cristina Ionica Oie, Balpreet Singh Ahluwalia, Gahl Levy, Christian Behrends, Sharon A. Tooze, Stephane Mouilleron, Trond Lamark, Terje Johansen
Summary: SAMM50 protein interacts with ATG8 family proteins and p62/SQSTM1 to act as a receptor for basal mitophagy, regulating mitochondrial architecture and quality control of MICOS components. SAMM50 and p62 cooperate to mediate efficient mitophagy upon metabolic switch to oxidative phosphorylation.
JOURNAL OF CELL BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Martina Wirth, Stephane Mouilleron, Wenxin Zhang, Eva Sjottem, Yakubu Princely Abudu, Ashish Jain, Hallvard Lauritz Olsvik, Jack-Ansgar Bruun, Minoo Razi, Harold B. J. Jefferies, Rebecca Lee, Dhira Joshi, Nicola O'Reilly, Terje Johansen, Sharon A. Tooze
Summary: Autophagy is a crucial degradative pathway for maintaining cellular homeostasis, with ATG8 proteins playing a central role in autophagosome formation and cytoplasmic cargo delivery. The binding specificity of ATG8 proteins with autophagy adaptors and receptors involves LIR motifs and phosphorylation. This study reveals the binding of a LIR motif in the Golgi protein SCOC to GABARAP, GABARAPL1, LC3A and LC3C, with phosphorylation regulating the affinity of LC3 family binding.
JOURNAL OF MOLECULAR BIOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Juncal Garcia-Garcia, Anne Kristin McLaren Berge, Katrine Stange Overa, Kenneth Bowitz Larsen, Zambarlal Bhujabal, Andreas Brech, Yakubu Princely Abudu, Trond Lamark, Terje Johansen, Eva Sjottem
Summary: TRIM27 is a multifunctional protein involved in various cellular functions. It has been found to facilitate mitochondrial clustering via SQSTM1/p62 and promote mitophagy by stabilizing phosphorylated TBK1 on mitochondria.
Review
Cell Biology
Nikoline Lander Rasmussen, Athanasios Kournoutis, Trond Lamark, Terje Johansen
Summary: NBR1 is an important autophagy receptor, serving as the main receptor in plants and co-existing with p62 in most animals. It participates in the selective autophagy of protein aggregates, and its mechanism and substrates are under investigation. Its roles in human diseases have also attracted attention.
JOURNAL OF CELL BIOLOGY
(2022)
Editorial Material
Cell Biology
Nikoline Lander Rasmussen, Jianwen Zhou, Hallvard Olsvik, Stephanie Kaeser-Pebernard, Trond Lamark, Joern Dengjel, Terje Johansen
Summary: TNIP1 is degraded through autophagy after infection to allow expression of inflammatory genes and proteins, and its levels rise again later to counteract sustained inflammatory signaling. The phosphorylation of a TNIP1 LIR motif by TBK1 regulates its selective autophagy.
Editorial Material
Cell Biology
Athanasios Kournoutis, Terje Johansen
Summary: The Atg8 family of autophagy proteins is found to have roles in both the cytoplasm and the cell nucleus. In a recent study, Jimenez-Moreno et al. (2023. J. Cell Biol.) discovered that nuclear LC3B interacts with the LIM homeodomain transcription factor LMX1B, serving as a cofactor for LMX1B-mediated transcription of autophagy genes. This interaction provides stress protection and ensures the survival of midbrain dopaminergic neurons.
JOURNAL OF CELL BIOLOGY
(2023)
Editorial Material
Biochemistry & Molecular Biology
Hallvard Lauritz Olsvik, Terje Johansen
Article
Multidisciplinary Sciences
Viola Nahse, Camilla Raiborg, Kia Wee Tan, Sissel Mork, Maria Lyngaas Torgersen, Eva Maria Wenzel, Mireia Nager, Veijo T. T. Salo, Terje Johansen, Elina Ikonen, Kay Oliver Schink, Harald Stenmark
Summary: DFCP1 is an ATPase located on omegasomes and plays a crucial role in selective autophagy by promoting the constriction of large omegasomes. It is essential for maintaining cellular homeostasis by removing damaged organelles and protein aggregates.
NATURE COMMUNICATIONS
(2023)
