Cytoskeleton (Hoboken, N.J.)最新文献_第5页

F-actin in the cuticular plate and junctions of auditory hair cells is regulated by ADF and cofilin to allow for normal stereocilia bundle patterning and maintenance. 听觉毛细胞角质板和连接处的 F-肌动蛋白受 ADF 和 cofilin 的调控，以实现正常的立体纤毛束模式化和维持。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-09-21 DOI: 10.1002/cm.21933

Jamis McGrath, Katelin Hawbaker, Benjamin J Perrin

{"title":"F-actin in the cuticular plate and junctions of auditory hair cells is regulated by ADF and cofilin to allow for normal stereocilia bundle patterning and maintenance.","authors":"Jamis McGrath, Katelin Hawbaker, Benjamin J Perrin","doi":"10.1002/cm.21933","DOIUrl":"10.1002/cm.21933","url":null,"abstract":"Auditory hair cells, which convert sound-induced vibrations in the inner ear into neural signals, depend on multiple actin populations for normal function. Stereocilia are mechanosensory protrusions formed around a core of linear, crosslinked F-actin. They are anchored in the cuticular plate, which predominantly consists of randomly oriented actin filaments. A third actin population is found near hair cell junctions, consisting of both parallel and branched filaments. Actin depolymerizing factor (ADF) and cofilin-1 (CFL1) proteins disassemble actin filaments and are required to regulate F-actin in stereocilia, but their effect on cuticular plate and junctional actin populations is unclear. Here, we show that loss of ADF and CFL1 disrupts the patterning of stereocilia into orderly bundles and that this phenotype correlates with defective development of the cuticular plate and junctional actin populations. ADF/CFL1 continue to regulate these actin populations in mature cells, which is necessary for long-term maintenance of hair cell morphology.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142302424","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

Introducing our Associate Editorial Board-Jayne Aiken, University of Pennsylvania, USA. 介绍我们的副编委--美国宾夕法尼亚大学的杰恩-艾肯（Jayne Aiken）。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-09-09 DOI: 10.1002/cm.21915

Paul Trevorrow, Jayne Aiken

引用次数: 0

Disruption of salt bridge interactions in the inter-domain cleft of the tubulin-like protein FtsZ of Escherichia coli makes cells sensitive to the cell division inhibitor PC190723. 大肠杆菌的类管蛋白 FtsZ 的结构域间隙中的盐桥相互作用被破坏，使细胞对细胞分裂抑制剂 PC190723 敏感。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-09-04 DOI: 10.1002/cm.21924

Sakshi Mahesh Poddar, Joyeeta Chakraborty, Pananghat Gayathri, Ramanujam Srinivasan

{"title":"Disruption of salt bridge interactions in the inter-domain cleft of the tubulin-like protein FtsZ of Escherichia coli makes cells sensitive to the cell division inhibitor PC190723.","authors":"Sakshi Mahesh Poddar, Joyeeta Chakraborty, Pananghat Gayathri, Ramanujam Srinivasan","doi":"10.1002/cm.21924","DOIUrl":"https://doi.org/10.1002/cm.21924","url":null,"abstract":"FtsZ forms a ring-like assembly at the site of division in bacteria. It is the first protein involved in the formation of the divisome complex to split the cell into two halves, indicating its importance in bacterial cell division. FtsZ is an attractive target for developing new anti-microbial drugs to overcome the challenges of antibiotic resistance. The most potent inhibitor against FtsZ is PC190723, which is effective against all strains and species of Staphylococcus, including the methicillin- and multi-drug-resistant Staphylococcus aureus and strains of Bacillus. However, FtsZs from bacteria such as E. coli, Streptococcus, and Enterococcus were shown to be resistant to this inhibitor. In this study, we provide further evidence that the three pairwise bridging interactions, between residues S227 and G191, R307 and E198 and D299 and R202, between S7, S9, S10 β-strands and the H7 helix occlude the inhibitor from binding to E. coli FtsZ. We generated single, double and triple mutations to disrupt those bridges and tested the effectiveness of PC190723 directly on Z-ring assembly in vivo. Our results show that the disruption of S227-G191 and R307-E198 bridges render EcFtsZ highly sensitive to PC190723 for Z-ring assembly. Ectopic expression of the double mutants, FtsZ S227I R307V results in hypersensitivity of the susceptible E. coli imp4213 strain to PC190723. Our studies could further predict the effectiveness of PC190723 or its derivatives towards FtsZs of other bacterial genera.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142127551","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

Evaluation of lamin A/C mechanotransduction under different surface topography in LMNA related muscular dystrophy. 评估 LMNA 相关性肌营养不良症患者在不同表面形貌下的层粘连 A/C机械传导。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-08-01 DOI: 10.1002/cm.21895

Subarna Dutta, T Muraganadan, Madavan Vasudevan

{"title":"Evaluation of lamin A/C mechanotransduction under different surface topography in LMNA related muscular dystrophy.","authors":"Subarna Dutta, T Muraganadan, Madavan Vasudevan","doi":"10.1002/cm.21895","DOIUrl":"https://doi.org/10.1002/cm.21895","url":null,"abstract":"Most of the single point mutations of the LMNA gene are associated with distinct muscular dystrophies, marked by heterogenous phenotypes but primarily the loss and symmetric weakness of skeletal muscle tissue. The molecular mechanism and phenotype-genotype relationships in these muscular dystrophies are poorly understood. An effort has been here to delineating the adaptation of mechanical inputs into biological response by mutant cells of lamin A associated muscular dystrophy. In this study, we implement engineered smooth and pattern surfaces of particular young modulus to mimic muscle physiological range. Using fluorescence and atomic force microscopy, we present distinct architecture of the actin filament along with abnormally distorted cell and nuclear shape in mutants, which showed a tendency to deviate from wild type cells. Topographic features of pattern surface antagonize the binding of the cell with it. Correspondingly, from the analysis of genome wide expression data in wild type and mutant cells, we report differential expression of the gene products of the structural components of cell adhesion as well as LINC (linkers of nucleoskeleton and cytoskeleton) protein complexes. This study also reveals mis expressed downstream signaling processes in mutant cells, which could potentially lead to onset of the disease upon the application of engineered materials to substitute the role of conventional cues in instilling cellular behaviors in muscular dystrophies. Collectively, these data support the notion that lamin A is essential for proper cellular mechanotransduction from extracellular environment to the genome and impairment of the muscle cell differentiation in the pathogenic mechanism for lamin A associated muscular dystrophy.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141876865","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 truncation mutant of adenomatous polyposis coli impairs apical cell extrusion through elevated epithelial tissue tension. 腺瘤性息肉病大肠杆菌的截短突变体会通过上皮组织张力的升高来影响顶端细胞的挤出。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-07-10 DOI: 10.1002/cm.21893

Wan J Gan, Rabina Giri, Jakob Begun, Helen E Abud, Edna C Hardeman, Peter W Gunning, Alpha S Yap, Ivar Noordstra

{"title":"A truncation mutant of adenomatous polyposis coli impairs apical cell extrusion through elevated epithelial tissue tension.","authors":"Wan J Gan, Rabina Giri, Jakob Begun, Helen E Abud, Edna C Hardeman, Peter W Gunning, Alpha S Yap, Ivar Noordstra","doi":"10.1002/cm.21893","DOIUrl":"https://doi.org/10.1002/cm.21893","url":null,"abstract":"Tissue tension encompasses the mechanical forces exerted on solid tissues within animal bodies, originating from various sources such as cellular contractility, interactions with neighboring cells and the extracellular matrix. Emerging evidence indicates that an imbalance in such forces can influence structural organization, homeostasis, and potentially contribute to disease. For instance, heightened tissue tension can impede apical cell extrusion, leading to the retention of apoptotic or transformed cells. In this study, we investigate the potential role of adenomatous polyposis coli (APC) in modulating tissue tension. Our findings reveal that expression of an APC truncation mutant elevates epithelial tension via the RhoA/ROCK pathway. This elevation induces morphological alterations and hampers apoptotic cell extrusion in cultured epithelial cells and organoids, both of which could be mitigated by pharmacologically restoring the tissue tension. This raises the possibility that APC mutations may exert pathogenetic effects by altering tissue mechanics.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141565310","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

Introducing our associate editorial board members: An interview with Nikki Reinemann. 介绍我们的副编辑委员会成员：尼基-莱纳曼访谈录

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-07-05 DOI: 10.1002/cm.21892

Paul Trevorrow, Nikki Reinemann

引用次数: 0

Toxoplasma replication is inhibited by MMV676477 without development of resistance. MMV676477 可抑制弓形虫的复制，但不会产生抗药性。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2024-05-16 DOI: 10.1002/cm.21876

Izra Abbaali, Danny Truong, Dawn M Wetzel, Naomi S Morrissette

{"title":"Toxoplasma replication is inhibited by MMV676477 without development of resistance.","authors":"Izra Abbaali, Danny Truong, Dawn M Wetzel, Naomi S Morrissette","doi":"10.1002/cm.21876","DOIUrl":"10.1002/cm.21876","url":null,"abstract":"Protozoan parasites cause life-threatening infections in both humans and animals, including agriculturally significant livestock. Available treatments are typically narrow spectrum and are complicated by drug toxicity and the development of resistant parasites. Protozoan tubulin is an attractive target for the development of broad-spectrum antimitotic agents. The Medicines for Malaria Pathogen Box compound MMV676477 was previously shown to inhibit replication of kinetoplastid parasites, such as Leishmania amazonensis and Trypanosoma brucei, and the apicomplexan parasite Plasmodium falciparum by selectively stabilizing protozoan microtubules. In this report, we show that MMV676477 inhibits intracellular growth of the human apicomplexan pathogen Toxoplasma gondii with an EC50 value of ~50 nM. MMV676477 does not stabilize vertebrate microtubules or cause other toxic effects in human fibroblasts. The availability of tools for genetic studies makes Toxoplasma a useful model for studies of the cytoskeleton. We conducted a forward genetics screen for MMV676477 resistance, anticipating that missense mutations would delineate the binding site on protozoan tubulin. Unfortunately, we were unable to use genetics to dissect target interactions because no resistant parasites emerged. This outcome suggests that future drugs based on the MMV676477 scaffold would be less likely to be undermined by the emergence of drug resistance.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11568068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140960164","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

An interview with Peter Gunning - School of Medical Sciences, UNSW Sydney, Australia. 采访彼得·甘宁-医学科学学院，新南威尔士大学悉尼，澳大利亚。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2022-04-01 Epub Date: 2022-07-22 DOI: 10.1002/cm.21715

Paul Trevorrow, Peter Gunning

引用次数: 0

Follow that cell: Leukocyte migration in L-plastin mutant zebrafish. 跟随细胞:l -活蛋白突变斑马鱼的白细胞迁移。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2022-04-01 Epub Date: 2022-07-22 DOI: 10.1002/cm.21717

John B Linehan, Jose Lucas Zepeda, Taylor A Mitchell, Elizabeth E LeClair

{"title":"Follow that cell: Leukocyte migration in L-plastin mutant zebrafish.","authors":"John B Linehan, Jose Lucas Zepeda, Taylor A Mitchell, Elizabeth E LeClair","doi":"10.1002/cm.21717","DOIUrl":"https://doi.org/10.1002/cm.21717","url":null,"abstract":"Actin assemblies are important in motile cells such as leukocytes which form dynamic plasma membrane extensions or podia. L-plastin (LCP1) is a leukocyte-specific calcium-dependent actin-bundling protein that, in mammals, is known to affect immune cell migration. Previously, we generated CRISPR/Cas9 engineered zebrafish lacking L-plastin (lcp1-/-) and reported that they had reduced survival to adulthood, suggesting that lack of L-plastin might negatively affect the immune system. To test this hypothesis, we examined the distribution and migration of neutrophils and macrophages in the transparent tail of early zebrafish larvae using cell-specific markers and an established wound-migration assay. Knockout larvae were similar to their heterozygous siblings in having equal body sizes and comparable numbers of neutrophils in caudal hematopoietic tissue at two days post-fertilization, indicating no gross defect in neutrophil production or developmental migration. When stimulated by a tail wound, all genotypes of neutrophils were equally migratory in a two-hour window. However for macrophages we observed both migration defects and morphological differences. L-plastin knockout macrophages still homed to wounds but were slower, less directional and had a star-like morphology with many leading and trailing projections. In contrast, wild type macrophages were faster, more directional, and had a more streamlined, slug-like morphology. Overall, these findings show that in larval zebrafish L-plastin knockout primarily affects the macrophage response with possible consequences for organismal immunity. Consistent with our observations, we propose a model in which cytoplasmic L-plastin negatively regulates macrophage integrin adhesion by holding these transmembrane heterodimers in a ‘clasped’, inactive form and is a necessary part of establishing macrophage polarity during chemokine-induced motility.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":"79 4-5","pages":"26-37"},"PeriodicalIF":0.0,"publicationDate":"2022-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40488845","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: 1

Meet the editorial staff: Interview series. 与编辑人员见面：访谈系列。

Cytoskeleton (Hoboken, N.J.) Pub Date : 2022-04-01 Epub Date: 2022-07-13 DOI: 10.1002/cm.21714

Paul Trevorrow

引用次数: 0