Mitochondrial Communications最新文献_第2页

Mitochondrial calcium transport during autophagy initiation 自噬启动过程中的线粒体钙运输

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.01.002

Sujyoti Chandra, Parul Katiyar, Aarooran S. Durairaj, Xinnan Wang

{"title":"Mitochondrial calcium transport during autophagy initiation","authors":"Sujyoti Chandra, Parul Katiyar, Aarooran S. Durairaj, Xinnan Wang","doi":"10.1016/j.mitoco.2024.01.002","DOIUrl":"10.1016/j.mitoco.2024.01.002","url":null,"abstract":"<div><p>While it has been shown that Ca<sup>2+</sup> dynamics at the ER membrane is essential for the initiation of certain types of autophagy such as starvation-induced autophagy, how mitochondrial Ca<sup>2+</sup> transport changes during the first stage of autophagy is not systemically characterized. An investigation of mitochondrial Ca<sup>2+</sup> dynamics during autophagy initiation may help us determine the relationship between autophagy and mitochondrial Ca<sup>2+</sup> fluxes. Here we examine acute mitochondrial and ER calcium responses to a panel of autophagy inducers in different cell types. Mitochondrial Ca<sup>2+</sup> transport and Ca<sup>2+</sup> transients at the ER membrane are triggered by different autophagy inducers. The mitophagy-inducer-initiated mitochondrial Ca<sup>2+</sup> uptake relies on mitochondrial calcium uniporter and may decelerate the following mitophagy. In neurons derived from a Parkinson's patient, mitophagy-inducer-triggered mitochondrial Ca<sup>2+</sup> influx is faster, which may slow the ensuing mitophagy.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 14-20"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000026/pdfft?md5=0543746d657e80e5c1b3bd64a36bd927&pid=1-s2.0-S2590279224000026-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139638700","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 protocol for detecting the cytoplasm-exposed mitochondrial DNA 检测细胞质暴露线粒体 DNA 的方案

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.09.001

Hao Liu , Haixia Zhuang , Lin Zeng , Jianming Xie , Kailun Qiu , Du Feng

引用次数: 0

Structure-destabilizing mutations unleash an intrinsic perforation activity of antiapoptotic Bcl-2 in the mitochondrial membrane enabling apoptotic cell death 结构失稳突变释放线粒体膜中抗凋亡Bcl-2的内在穿孔活性，导致细胞凋亡

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.08.001

Ping Gao , Zhi Zhang , Rui Wang , Li Huang , Hao Wu , Zhenzhen Qiao , Xiaohui Wang , Haijing Jin , Jun Peng , Lei Liu , Quan Chen , Jialing Lin

{"title":"Structure-destabilizing mutations unleash an intrinsic perforation activity of antiapoptotic Bcl-2 in the mitochondrial membrane enabling apoptotic cell death","authors":"Ping Gao , Zhi Zhang , Rui Wang , Li Huang , Hao Wu , Zhenzhen Qiao , Xiaohui Wang , Haijing Jin , Jun Peng , Lei Liu , Quan Chen , Jialing Lin","doi":"10.1016/j.mitoco.2023.08.001","DOIUrl":"https://doi.org/10.1016/j.mitoco.2023.08.001","url":null,"abstract":"<div><p>Bcl-2 and Bax share a similar structural fold in solution, yet function oppositely in the mitochondrial outer membrane (MOM) during apoptosis. The proapoptotic Bax forms pores in the MOM to trigger cell death, whereas Bcl-2 inhibits the Bax pore formation to prevent cell death. Intriguingly both proteins can switch to a similar conformation after activation by BH3-only proteins, with multiple regions embedded in the MOM. Here we tested a hypothesis that destabilization of the Bcl-2 structure might convert Bcl-2 to a Bax-like perforator. We discovered that mutations of glutamate 152 which eliminate hydrogen bonds in the protein core and thereby reduce the Bcl-2 structural stability. These Bcl-2 mutants induced apoptosis by releasing cytochrome <em>c</em> from the mitochondria in the cells that lack Bax and Bak, the other proapoptotic perforator. Using liposomal membranes made with typical mitochondrial lipids and reconstituted with purified proteins we revealed this perforation activity was intrinsic to Bcl-2 and could be unleashed by a BH3-only protein, similar to the perforation activity of Bax. Our study thus demonstrated a structural conversion of antiapoptotic Bcl-2 to a proapoptotic perforator through a simple molecular manipulation or interaction that is worthy to explore further for eradicating cancer cells that are resistant to a current Bcl-2-targeting drug.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"1 ","pages":"Pages 48-61"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50192437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A brief introduction to the history of mitochondrial research in Japan 日本线粒体研究史简介

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.02.001

Yasutoshi Koga , Masashi Tanaka

引用次数: 0

TELP theory: Elucidating the major observations of Rieger et al. 2021 in mitochondria TELP理论：阐明Rieger等人2021在线粒体中的主要观察结果

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.09.001

James Weifu Lee

引用次数: 0

Mitochondria: The hot organelles are getting hotter 线粒体：热的细胞器越来越热

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2022.10.001

Quan Chen

引用次数: 0

Role of TFEB and TFE3 in mediating lysosomal and mitochondrial adaptations to contractile activity in skeletal muscle myotubes TFEB和TFE3在介导溶酶体和线粒体对骨骼肌肌管收缩活性适应中的作用

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.10.001

Ashley N. Oliveira , Yuki Tamura , Jonathan M. Memme , David A. Hood

{"title":"Role of TFEB and TFE3 in mediating lysosomal and mitochondrial adaptations to contractile activity in skeletal muscle myotubes","authors":"Ashley N. Oliveira , Yuki Tamura , Jonathan M. Memme , David A. Hood","doi":"10.1016/j.mitoco.2023.10.001","DOIUrl":"https://doi.org/10.1016/j.mitoco.2023.10.001","url":null,"abstract":"<div><p>Exercise is potent stimulus for mitochondrial adaptations, serving to activate mitochondrial biogenesis as well as mitochondrial turnover. Through the process of mitophagy, dysfunctional mitochondria are selectively targeted and recycled via the lysosomes, which is activated following a single bout of exercise. The microphthalamia (MiT) family of transcription factors, including TFEB and TFE3, are widely recognized as the master regulators of lysosomal biogenesis, as they homo- and hetero-dimerize to transcriptionally regulate lysosomal and macroautophagy-related genes. It is currently unknown to what extent TFEB and TFE3 regulate mitophagy, and whether these transcription factors mediate mitochondrial adaptations to contractile activity (CA). Here we show that following an acute bout of contractile activity in cultured C2C12 murine skeletal muscle myotubes, LC3-II mitophagy flux is induced and the absence of TFEB or TFE3 impairs this acute mitophagic response. However, the loss of either transcription factor alone does not mitigate the improvements in oxygen consumption seen following chronic contractile activity (CCA). Chronic contractile activity also elicited functional improvements in lysosomes including a reduction in size and increased proteolytic activity, evidenced by increased digestion and unquenching of DQ-BSA fluorophore, thereby illustrating a level of redundancy between the two transcription factors in mediating chronic contractile activity-induced adaptations. However, in the absence of both TFEB and TFE3, lysosomal adaptations were not observed following chronic contractile activity and subsequent mitochondrial adaptations were attenuated. These findings underscore the importance of the lysosomes, and of TFEB and TFE3, in mediating mitochondrial adaptations to chronic contractile activity.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"1 ","pages":"Pages 73-87"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50192439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A novel mitochondrial quality control pathway: Autophagic secretion of mitochondria (ASM) 一种新的线粒体质量控制途径：线粒体自噬分泌（ASM）

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2022.12.001

Hayden Weng Siong Tan , Guang Lu , Han-Ming Shen

引用次数: 0

Correcting abnormal mitochondrial dynamics to facilitate tumor treatment 纠正线粒体动力学异常促进肿瘤治疗

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.07.001

Bowen Yang, Yumeng Lin, Ying-Qiang Shen

引用次数: 1

Fusion activators enhance mitochondrial function 融合激活剂增强线粒体功能

Mitochondrial Communications Pub Date : 2023-01-01 DOI: 10.1016/j.mitoco.2023.03.001

William M. Rosencrans, David C. Chan

引用次数: 0