Mitochondrial Communications最新文献_第2页

Is localized chemiosmosis necessary in mitochondria? Is Lee's TELP protonic capacitor hypothesis a reasonable model? 线粒体中的局部化合作用是否必要？李的 TELP 质子电容器假说是一个合理的模型吗？

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.06.001

Todd P. Silverstein

{"title":"Is localized chemiosmosis necessary in mitochondria? Is Lee's TELP protonic capacitor hypothesis a reasonable model?","authors":"Todd P. Silverstein","doi":"10.1016/j.mitoco.2024.06.001","DOIUrl":"https://doi.org/10.1016/j.mitoco.2024.06.001","url":null,"abstract":"<div><p>Recent high-resolution pH measurements in mitochondria show ΔpH across the F<sub>1</sub>F<sub>0</sub> ATP synthase to be quite low, 0.07–0.32. Our meta-analysis of published values of transmembrane potential (<span><math><mrow><mo>Δ</mo><mi>ψ</mi></mrow></math></span>) shows it to be identical in vivo and in vitro: -159 ± 16 mV. With the low ΔpH, the thermodynamic efficiency of proton-driven ATP synthesis exceeds 100 % for average- and low-potential (−123 mV) mitochondria, and possibly also for high-potential (−180 mV) mitochondria. Efficiencies exceeding 100 % may violate the second law of thermodynamics, and suggest a need for localized chemiosmosis, i.e., the existence of a membrane surface ΔpH that exceeds the bulk phase ΔpH by at least 0.2 units in high-potential mitochondria, and by 1.1 units in low-potential mitochondria. The lack of equilibration between protons in the bulk phase and those at the membrane surface is explained by two models which we discuss and compare: the potential well/barrier model, and the TELP protonic capacitor model.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 48-57"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000051/pdfft?md5=ed06f95ee11648d4c7f30933cafa6792&pid=1-s2.0-S2590279224000051-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141303240","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

Defective biogenesis of human mitochondrial ribosomes causes sensorineural deafness 人类线粒体核糖体生物生成缺陷导致感音神经性耳聋

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.11.001

Chao Chen Ph.D. , Wenqi Shan , Min-Xin Guan Ph.D.

{"title":"Defective biogenesis of human mitochondrial ribosomes causes sensorineural deafness","authors":"Chao Chen Ph.D. , Wenqi Shan , Min-Xin Guan Ph.D.","doi":"10.1016/j.mitoco.2024.11.001","DOIUrl":"10.1016/j.mitoco.2024.11.001","url":null,"abstract":"<div><div>Thirteen proteins of oxidative phosphorylation complexes encoded by mitochondrial DNA (mtDNA) were synthesized by own specific ribosomes (mitoribosomes). Mitoribosomes composed of nucleus-encoding proteins and mtDNA-encoding 12S and 16S ribosomal RNA. They are linked with sensorineural deafness and the targets of aminoglycosides. Mutations in nuclear genes encoding mitoribosome subunits cause syndromic deafness. The 12S rRNA 1555A > G and 1494C > T mutations have been associated with aminoglycoside-induced and nonsyndromic deafness in many families worldwide. These mutations create 1494C-G1555 or 1494U-A1555 base-pair at the A-site of 12S rRNA, make ribosomes more bacteria-like, thereby altering the binding for aminoglycosides and translation. These mutations conferred to mild mitochondrial dysfunctions, thereby requiring genetic and environmental factors to produce a deafness phenotype. The administration of aminoglycosides induces deafness in these subjects carrying the 12S rRNA mutations. Nuclear modifier including TRMU and mitochondrial modifier contributed to the tissue-specific phenotypic manifestation of 12S rRNA mutations. Especially, hair cell-like cells differentiated from patients-derived iPSCs harboring both m.1555A > G and TRMU c.28G > T mutations displayed greater defects in the morphology and functions than those in cells bearing only m.1555A > G mutation and these defects were restored by genetic correction of TRMU c.28G > T mutation. These provide new insights into pathophysiology of deafness, genetic counseling, prevention and therapeutic interventions for this disease.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 114-122"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142706268","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

Structural determinants of mitochondrial STAT3 targeting and function 线粒体 STAT3 靶向和功能的结构决定因素

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.01.001

Isabelle J. Marié , Tanaya Lahiri , Özlem Önder , Kojo S.J. Elenitoba-Johnson , David E. Levy

{"title":"Structural determinants of mitochondrial STAT3 targeting and function","authors":"Isabelle J. Marié , Tanaya Lahiri , Özlem Önder , Kojo S.J. Elenitoba-Johnson , David E. Levy","doi":"10.1016/j.mitoco.2024.01.001","DOIUrl":"10.1016/j.mitoco.2024.01.001","url":null,"abstract":"<div><p>Signal transducer and activator of transcription (STAT) 3 has been found within mitochondria in addition to its canonical role of shuttling between cytoplasm and nucleus during cytokine signaling. Mitochondrial STAT3 has been implicated in modulation of cellular metabolism, largely through effects on the respiratory electron transport chain. However, the structural requirements underlying mitochondrial targeting and function have remained unclear. Here, we show that mitochondrial STAT3 partitions between mitochondrial compartments defined by differential detergent solubility, suggesting that mitochondrial STAT3 is membrane associated. The majority of STAT3 was found in an SDS soluble fraction copurifying with respiratory chain proteins, including numerous components of the complex I NADH dehydrogenase, while a minor component was found with proteins of the mitochondrial translation machinery. Mitochondrial targeting of STAT3 required the amino-terminal domain, and an internal linker domain motif also directed mitochondrial translocation. However, neither the phosphorylation of serine 727 nor the presence of mitochondrial DNA was required for the mitochondrial localization of STAT3. Two cysteine residues in the STAT3 SH2 domain, which have been previously suggested to be targets for protein palmitoylation, were also not required for mitochondrial translocation, but were required for its function as an enhancer of complex I activity. These structural determinants of STAT3 mitochondrial targeting and function provide potential therapeutic targets for disrupting the activity of mitochondrial STAT3 in diseases such as cancer.</p></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 1-13"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2590279224000014/pdfft?md5=0cbb61fa14ca122b7f046fd145ac06aa&pid=1-s2.0-S2590279224000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139455625","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

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

Sex differences in the genetics of autism spectrum disorder and their impact on gene expression associated with mitochondrial function

Mitochondrial Communications Pub Date : 2024-01-01 DOI: 10.1016/j.mitoco.2024.12.001

María de los Angeles Carcamo , Rodrigo A. Quintanilla , William Tiznado , Lina M. Ruiz

{"title":"Sex differences in the genetics of autism spectrum disorder and their impact on gene expression associated with mitochondrial function","authors":"María de los Angeles Carcamo , Rodrigo A. Quintanilla , William Tiznado , Lina M. Ruiz","doi":"10.1016/j.mitoco.2024.12.001","DOIUrl":"10.1016/j.mitoco.2024.12.001","url":null,"abstract":"<div><div>Autism spectrum disorder (ASD) is a neurodevelopmental condition that affects social-communicative skills and is characterized by restricted and stereotyped behaviors. It affects more males, with a ratio of 4:1, and has a prevalence of 1:54 children. Manifestations of ASD vary by gender, with specific behaviors less pronounced in females. Using data from the Gene Expression Omnibus repository, this research explored sex-related genetic differences in ASD and their impact on mitochondrial gene expression. Peripheral blood DNA was found to exhibit differential methylation patterns by sex, with additional alterations in individuals with ASD. Sex-specific transcriptional changes were also identified in cord blood from high-risk ASD pregnancies. Of 50 genes with differential methylation by sex, only the <em>PLEKHN1</em> gene is related to mitochondrial function. Age correlated with symptoms and diagnosis in males, whereas <em>PLEKHN1</em> methylation was associated with age and internalizing symptoms in females. In conclusion, sex influences genetic contributions in ASD, affecting mitochondrial gene expression.</div></div>","PeriodicalId":100931,"journal":{"name":"Mitochondrial Communications","volume":"2 ","pages":"Pages 129-139"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143973","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