Autophagy reports最新文献_第4页

Autophagy reports Pub Date : 2024-10-15 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2395731

Morten Petersen, Tamar Avin-Wittenberg, Diane C Bassham, Yasin Dagdas, Chudi Fan, Alisdair R Fernie, Liwen Jiang, Divya Mishra, Marisa S Otegui, Eleazar Rodriguez, Daniel Hofius

{"title":"Autophagy in plants.","authors":"Morten Petersen, Tamar Avin-Wittenberg, Diane C Bassham, Yasin Dagdas, Chudi Fan, Alisdair R Fernie, Liwen Jiang, Divya Mishra, Marisa S Otegui, Eleazar Rodriguez, Daniel Hofius","doi":"10.1080/27694127.2024.2395731","DOIUrl":"10.1080/27694127.2024.2395731","url":null,"abstract":"Autophagy is a process of cellular self-eating, which allows organisms to eliminate and recycle unwanted components and damaged organelles to maintain cellular homeostasis. It is an important process in the development of eukaryotic organisms. Autophagy plays a critical role in many physiological processes in plants such as nutrient remobilization, cell death, immunity, and abiotic stress responses. Autophagy thus represents an obvious target for generating resilient crops. During plant development, autophagy is also implicated in the differentiation and maturation of various cell types and plant organs, including root cap cells, tracheary elements, gametes, fruits and seeds. Here, we review our current understanding and recent advances of plant autophagy including insight into autophagy regulation and signaling as well as autophagosome membrane biogenesis. In addition, we describe how autophagy contributes to development, metabolism, biotic and abiotic stress tolerance and where the autophagic field is heading in terms of applied research for crop improvement.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2395731"},"PeriodicalIF":0.0,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ATG5 is dispensable for ATG8ylation of cellular proteins. ATG5对于细胞蛋白的atg8化是不可缺少的。

Autophagy reports Pub Date : 2024-10-12 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2392450

Robin Ketteler, Koshiro Kiso, Lucas von Chamier, Alexander Agrotis

{"title":"ATG5 is dispensable for ATG8ylation of cellular proteins.","authors":"Robin Ketteler, Koshiro Kiso, Lucas von Chamier, Alexander Agrotis","doi":"10.1080/27694127.2024.2392450","DOIUrl":"10.1080/27694127.2024.2392450","url":null,"abstract":"Protein ATG8ylation refers to a post-translational modification involving covalent attachment of ubiquitin-like autophagy-related protein ATG8 (LC3/GABARAP) to other cellular proteins, with reversal mediated by ATG4 proteases. While lipid ATG8ylation is important for autophagosome formation and mechanistically well-characterized, little is known about the mechanism of protein ATG8ylation. Here, we investigated the conjugation machinery of protein ATG8ylation in CRISPR/Cas9-engineered knockout human cell lines, utilizing a deconjugation-resistant (Q116P G120) form of MAP1LC3B. We report that protein ATG8ylation requires the E1-like activating enzyme ATG7 and E2-like conjugating enzyme ATG3, in common with ATG8 lipidation. However, in contrast, the E3-like ATG12-ATG5-ATG16L1 complex involved in lipidation is dispensable for protein ATG8ylation, since ATG5 knockout cells can form ATG8ylated protein conjugates. Further, we uncover that ATG7 itself is a target of ATG8ylation. Overall, our work provides crucial insight into the mechanism of protein ATG8ylation, distinguishing it from ATG8 lipidation, which will aid investigating its functional role.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2392450"},"PeriodicalIF":0.0,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864658/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Getting PIKy with the lysosome membrane (again). 用溶酶体膜（再次）得到PIKy。

Autophagy reports Pub Date : 2024-10-12 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2412916

Alison D Klein, Michael Overholtzer

引用次数: 0

Truncated tau disrupts autophagy and endolysosomal systems. 截短的tau破坏自噬和内溶酶体系统。

Autophagy reports Pub Date : 2024-10-08 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2409563

Saskia J Pollack, Diane P Hanger, Wendy Noble, Maria Jimenez-Sanchez

引用次数: 0

A redox-independent stress response mediated by phase-separated SQSTM1/p62. 相分离SQSTM1/p62介导的不依赖氧化还原的应激反应。

Autophagy reports Pub Date : 2024-10-07 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2383088

Yoshinobu Ichimura, Masaaki Komatsu

{"title":"A redox-independent stress response mediated by phase-separated SQSTM1/p62.","authors":"Yoshinobu Ichimura, Masaaki Komatsu","doi":"10.1080/27694127.2024.2383088","DOIUrl":"10.1080/27694127.2024.2383088","url":null,"abstract":"The KEAP1 (kelch like ECH associated protein 1)- NFE2L2/NRF2 (NFE2 like bZIP transcription factor 2) pathway is a major antioxidative stress pathway that contributes to cellular homeostasis. KEAP1 acts as a sensor and attenuates degradation of the transcription factor NRF2, which induces gene expression for a network of enzymes involved in the antioxidant response. When cells are exposed to various electrophiles and reactive oxidative species, they modify one or more selective cysteine residues in KEAP1, resulting in conformational changes that disable its NRF2-inhibitory function. In addition to this redox-dependent pathway, SQSTM1/p62 (sequestosome 1), which is a selective autophagy receptor for ubiquitinated proteins and a driver of liquid-liquid phase separation (LLPS) upon binding to ubiquitinated proteins, competitively inhibits the binding between KEAP1 and NRF2, thereby disabling the NRF2-repressive function of KEAP1. Our study showed that phase-separated SQSTM1/p62 bodies are phosphorylated by ULK1 (Unc-51 like autophagy activating kinase 1) and that KEAP1 is retained in the SQSTM1/p62 body, resulting in NRF2-activation in a redox-independent manner.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2383088"},"PeriodicalIF":0.0,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864652/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neuronal activity triggers secretory autophagy to mediate the extracellular release of SNCA/α-synuclein. 神经元活动触发分泌性自噬介导SNCA/α-突触核蛋白的细胞外释放。

Autophagy reports Pub Date : 2024-10-07 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2410683

Yoshitsugu Nakamura, Shigeki Arawaka

{"title":"Neuronal activity triggers secretory autophagy to mediate the extracellular release of SNCA/α-synuclein.","authors":"Yoshitsugu Nakamura, Shigeki Arawaka","doi":"10.1080/27694127.2024.2410683","DOIUrl":"10.1080/27694127.2024.2410683","url":null,"abstract":"Autophagy has two distinct pathways, degradation and secretion. Autophagic degradation plays a pivotal role in cellular homeostasis by the formation of a double-membrane autophagosome in concert with numerous ATG (autophagy-related) proteins. However, the mechanism that mediates autophagic secretion is not fully understood. To explore how autophagic secretion is physiologically triggered and regulated in neurons, we investigated whether neuronal activity affected autophagic secretion by analyzing SNCA secretion in mouse primary cortical neurons and SH-SY5Y cells. In primary neurons, rapamycin promoted SNCA secretion, while the effect was canceled in primary neurons of Becn1 +/-deficient mice. Stimulating neuronal activity by glutamate promoted SNCA secretion, autophagic flux, and colocalization of SNCA with LC3 (microtubule-associated proteins 1 light chain 3). These effects were inhibited by the intracellular Ca2+ chelator BAPTA-AM. Additionally, glutamate-induced SNCA secretion was suppressed by Atg5 or Rab8a knockdown in SH-SY5Y cells, and mainly occurred in the fashion associated with extracellular vesicles in primary neurons. These results suggest that neuronal activity triggers autophagic secretion for releasing SNCA via an increase in intracellular Ca2+ concentration.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2410683"},"PeriodicalIF":0.0,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Methods for detection of cardiac glycogen-autophagy. 心糖原自噬的检测方法。

Autophagy reports Pub Date : 2024-09-22 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2405331

Parisa Koutsifeli, Lorna J Daniels, Joshua Neale, Sarah Fong, Upasna Varma, Marco Annandale, Xun Li, Yohanes Nursalim, James R Bell, Kate L Weeks, Aleksandr Stotland, David J Taylor, Roberta A Gottlieb, Lea M D Delbridge, Kimberley M Mellor

{"title":"Methods for detection of cardiac glycogen-autophagy.","authors":"Parisa Koutsifeli, Lorna J Daniels, Joshua Neale, Sarah Fong, Upasna Varma, Marco Annandale, Xun Li, Yohanes Nursalim, James R Bell, Kate L Weeks, Aleksandr Stotland, David J Taylor, Roberta A Gottlieb, Lea M D Delbridge, Kimberley M Mellor","doi":"10.1080/27694127.2024.2405331","DOIUrl":"10.1080/27694127.2024.2405331","url":null,"abstract":"Glycogen-autophagy ('glycophagy') is a selective autophagy process involved in delivering glycogen to the lysosome for bulk degradation. Glycophagy protein intermediaries include STBD1 as a glycogen tagging receptor, delivering the glycogen cargo into the forming phagosome by partnering with the Atg8 homolog, GABARAPL1. Glycophagy is emerging as a key process of energy metabolism and development of reliable tools for assessment of glycophagy activity is an important priority. Here we show that antibodies raised against the N-terminus of the GABARAPL1 protein (but not the full-length protein) detected a specific endogenous GABARAPL1 immunoblot band at 18kDa. A stable GFP-GABARAPL1 cardiac cell line was used to quantify GABARAPL1 lysosomal flux via measurement of GFP puncta in response to lysosomal inhibition with bafilomycin. Endogenous glycophagy flux was quantified in primary rat ventricular myocytes by the extent of glycogen accumulation with bafilomycin combined with chloroquine treatment (no effect observed with bafilomycin or chloroquine alone). In wild-type isolated mouse hearts, bafilomycin alone and bafilomycin combined with chloroquine (but not chloroquine alone) elicited a significant increase in glycogen content signifying basal glycophagy flux. Collectively, these methodologies provide a comprehensive toolbox for tracking cardiac glycophagy activity to advance research into the role of glycophagy in health and disease.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2405331"},"PeriodicalIF":0.0,"publicationDate":"2024-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The selective autophagic degradation of avian metapneumovirus subgroup C M2-2 protein via SQSTM1 suppresses viral replication. 禽偏肺病毒C亚群M2-2蛋白通过SQSTM1选择性自噬降解抑制病毒复制。

Autophagy reports Pub Date : 2024-09-21 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2375936

Lei Hou, Jinshuo Guo, Jianwei Zhou, Jue Liu

引用次数: 0

Photo-protective role of ATG5/ATG7-independent alternative autophagy in human keratinocytes. ATG5/ atg7非依赖性自噬在人角质形成细胞中的光保护作用。

Autophagy reports Pub Date : 2024-09-05 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2396212

Tatsuya Hasegawa, Masaya Nakashima, Satoru Torii, Shinya Honda, Shigeomi Shimizu

{"title":"Photo-protective role of ATG5/ATG7-independent alternative autophagy in human keratinocytes.","authors":"Tatsuya Hasegawa, Masaya Nakashima, Satoru Torii, Shinya Honda, Shigeomi Shimizu","doi":"10.1080/27694127.2024.2396212","DOIUrl":"10.1080/27694127.2024.2396212","url":null,"abstract":"Excessive exposure to sunlight, especially to ultraviolet B (UVB), results in DNA damage and a cutaneous inflammatory reaction commonly known as sunburn, which increases skin cancer risks. UVB-induced inflammasome activation in epidermal keratinocytes mediates the cutaneous inflammatory response, but the intracellular machinery that maintains skin homeostasis by suppressing UVB-induced inflammasome activation is unclear. Here, we summarize our recent work on the protective role of alternative autophagy against UVB-induced NLRP3 (NLR family pyrin domain containing 3) inflammasome activation in human keratinocytes. We found that UVB radiation induces ATG5/ATG7-independent alternative (noncanonical) autophagy, which leads to suppression of NLRP3 inflammasome activation through the clearance of damaged mitochondria in UVB-irradiated keratinocytes. Our findings indicate that ATG5/ATG7-independent alternative autophagy, rather than conventional autophagy, may play a key role in mitigating inflammatory responses, and restoring skin homeostasis after UV radiation.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2396212"},"PeriodicalIF":0.0,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864719/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue. 脂肪组织健康转化过程中铁通量的肝-脂肪串扰。

Autophagy reports Pub Date : 2024-09-04 eCollection Date: 2024-01-01 DOI: 10.1080/27694127.2024.2396696

Jinying Yang, Limin Shi, Anna L Cubito, James F Collins, Zhiyong Cheng

{"title":"A liver-fat crosstalk for iron flux during healthy beiging of adipose tissue.","authors":"Jinying Yang, Limin Shi, Anna L Cubito, James F Collins, Zhiyong Cheng","doi":"10.1080/27694127.2024.2396696","DOIUrl":"10.1080/27694127.2024.2396696","url":null,"abstract":"Beiging of adipocytes is characteristic of a higher number of mitochondria, the central hub of metabolism in the cell. However, studies show that beiging can improve metabolic health or cause metabolic disorders. Here we discuss a liver-fat crosstalk for iron flux associated with healthy beiging of adipocytes. Deletion of the transcription factor FoxO1 in adipocytes (adO1KO mice) induces a higher iron flux from the liver to white adipose tissue, concurrent with augmented mitochondrial biogenesis that increases iron demands. In addition, adO1KO mice adopt an alternate mechanism to sustain mitophagy, which enhances mitochondrial quality control, thereby improving mitochondrial respiratory capacity and metabolic health. However, the liver-fat crosstalk is not detectable in adipose Atg7 knockout (ad7KO) mice, which undergo beiging of adipocytes but have metabolic dysregulation. Autophagic clearance of mitochondria is blocked in ad7KO mice, which accumulates dysfunctional mitochondria and elevates mitochondrial content but lowers mitochondrial respiratory capacity. Mitochondrial biogenesis is comparable in the control and ad7KO mice, and the iron influx into adipocytes and iron efflux from the liver remain unchanged. Therefore, activation of the liver-fat crosstalk is critical for mitochondrial quality control that underlies healthy beiging of adipocytes.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"3 1","pages":"2396696"},"PeriodicalIF":0.0,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864716/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144112820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0