Cytoskeleton (Hoboken, N.J.)最新文献_第4页

Picture of the Month by Arif Ashraf. Arif Ashraf的月度图片。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-06-01 Epub Date: 2026-06-08 DOI: 10.1002/cm.70157

引用次数: 0

Imaging and Assessment Methods of Phenotyping Osteocyte Networks. 骨细胞网络表型的成像和评估方法。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-06-01 DOI: 10.1002/cm.70152

Rosa M Guerra, Mia Nie, X Lucas Lu, Velia M Fowler, Liyun Wang

{"title":"Imaging and Assessment Methods of Phenotyping Osteocyte Networks.","authors":"Rosa M Guerra, Mia Nie, X Lucas Lu, Velia M Fowler, Liyun Wang","doi":"10.1002/cm.70152","DOIUrl":"https://doi.org/10.1002/cm.70152","url":null,"abstract":"Osteocytes, the master orchestrators of bone remodeling, form an extensive network of F-actin rich dendrites that enable them to sense external mechanical signals and communicate with other cells, which are essential to maintain bone homeostasis and bone mass. Loss of the osteocyte dendrite number and connectivity and similar changes in the lacunar-canalicular pore system (LCS) surrounding the osteocyte dendrites have been reported in aged animals and humans. Increasing evidence demonstrates the close association of osteocyte dendrites/LCS alterations with many bone disorders and diseases that affect the formation, maturation, maintenance, or degeneration of osteocyte dendrites. Given their intrinsic temporal and spatial variations, phenotyping the osteocyte dendrite/LCS requires rigorous evaluation of a large number of cells with reliable methods. The goal of this manuscript is to describe several easy-to-adopt strategies of phenotyping osteocyte dendrites and high-throughput analysis methods developed in previous literature and our laboratories. Protocols will be detailed for (1) preparing various murine and human bone samples; (2) fluorescence staining of the dendrite cytoskeleton; (3) silver nitrate staining of the LCS; and (4) sample imaging and analysis including macro plugins using the free software ImageJ. The protocols provide reliable methods to phenotyping osteocytes in the context of aging, diseases, and treatments.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148139960","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

Antagonistic Relationship Between Microtubule-Stabilizing and Destabilizing Factors for the Maintenance of Axonal Microtubule Dynamics and Polarity in C. elegans Touch Neuron. 微管稳定和不稳定因素在线虫触摸神经元轴突微管动力学和极性维持中的拮抗关系。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-05-18 DOI: 10.1002/cm.70145

Dharmendra Puri, Sunanda Sharma, Anindya Ghosh-Roy

{"title":"Antagonistic Relationship Between Microtubule-Stabilizing and Destabilizing Factors for the Maintenance of Axonal Microtubule Dynamics and Polarity in C. elegans Touch Neuron.","authors":"Dharmendra Puri, Sunanda Sharma, Anindya Ghosh-Roy","doi":"10.1002/cm.70145","DOIUrl":"10.1002/cm.70145","url":null,"abstract":"Proper regulation of microtubule (MT) cytoskeleton forms the basis for molecular and functional polarization of neurons. The optimal growth of mechanosensory neurons in C. elegans depends on the activity of the microtubule depolymerizing enzyme, Kinesin-13/KLP-7. Yet it's unclear how KLP-7 collaborates with other microtubule regulators in neurons for proper MT regulation. Using the ectopic growth of mechanosensory neurons in klp-7 mutants as a phenotypic handle, we characterized its genetic interactions with known microtubule stabilizers. We found that mutations in unc-33(CRMP-2), unc-44(Ankyrin), or components of the unc-14/unc-51/vab-8 pathway suppress klp-7(0) ectopic growth. Quantification of EBP-2::GFP dynamics revealed that these factors promote microtubule stability in axon-like PLM anterior neurites, suggesting an antagonistic role to KLP-7. Additionally, mec-7 (β-tubulin), unc-33, and unc-44 proteins promote the plus-end-out microtubule polarity in these neurites, and their loss in klp-7(0) mutant can reciprocally suppress the microtubule dynamics defects observed in single mutants. Notably, the simultaneous loss of klp-7 and mec-7 restored steady-state microtubule dynamics and wild-type-like PLM morphology. Together, our findings suggest that the antagonistic interplay between microtubule depolymerizing kinesin KLP-7 and microtubule-stabilizing factors, UNC-44, UNC-33, and tubulins, is necessary to maintain steady-state microtubule dynamics and plus-end-out axonal microtubule polarity in neurons.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":"e70145"},"PeriodicalIF":1.6,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147977635","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

Foundational Discoveries in Actin Regulation: An Interview With Tom Pollard. 肌动蛋白调控的基础发现：采访Tom Pollard。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-05-17 DOI: 10.1002/cm.70146

Alfred C Chin, Eva P Karasmanis

引用次数: 0

Emerging Mechanobiological Roles of LIM-Only Proteins: Distinct Pathways of CRP and LMO in Cytoskeleton Regulation and Disease. 仅limo蛋白的新机制生物学作用：CRP和LMO在细胞骨架调节和疾病中的不同途径。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-05-13 DOI: 10.1002/cm.70151

Sakshi Jain, Rounab Sarkar, Kashish Salian, Upendra Nongthomba

{"title":"Emerging Mechanobiological Roles of LIM-Only Proteins: Distinct Pathways of CRP and LMO in Cytoskeleton Regulation and Disease.","authors":"Sakshi Jain, Rounab Sarkar, Kashish Salian, Upendra Nongthomba","doi":"10.1002/cm.70151","DOIUrl":"https://doi.org/10.1002/cm.70151","url":null,"abstract":"Mechanotransduction is a process in which cells sense extracellular cues from their microenvironment and convert mechanical changes into biochemical signals, thereby regulating gene expression and various cellular processes. LIM-domain proteins have recently been identified as essential players in several mechanotransduction pathways. They have been shown to bind tensed actin filaments, which are enriched at focal adhesions, and to regulate various cellular signalling pathways by shuttling between the cytoplasm and the nucleus. Mainly, the stress sensitivity of the selected LIM proteins is demonstrated in contractile stress fibres and focal adhesion in fibroblasts, with the presence of at least three LIM domains required for force-induced interaction with stressed actin filaments. However, recent studies have expanded our understanding by identifying the LIM-only class of these proteins (LMOs), which contain only two LIM domains, at keratin intermediate filaments in epithelial cells, indicating their importance as signalling hubs in mechanotransduction pathways. In addition, members of the CRP class of LIM domain proteins with only two LIM domains linked to a short glycine-rich repeat can directly bind F-actin even in the absence of mechanical load and can also recruit to the stress fibres in response to stretch. Their dysregulation is linked with several pathological conditions, like cancer metastasis, cardiovascular disorders, muscle disorders, and inflammatory disorders, emphasising their importance in disease progression. This review highlights the diverse roles of LIM-only proteins, LMOs & CRPs in mechanotransduction, emphasising their emerging significance in integrating cytoskeleton dynamics with gene expression and the therapeutic potential of targeting LIM-only proteins to modulate the mechanotransduction pathway in a clinical context.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147935994","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

Dpcd Induces Hydrocephalus Because of Partial Defects in the Inner Dynein Arms, With Abnormal Ciliary Motility. Dpcd引起脑积水是由于内动力臂部分缺陷，伴有纤毛运动异常。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-05-01 Epub Date: 2025-07-28 DOI: 10.1002/cm.70012

Taiki Yamamoto, Kazuhito Takeuchi, Yuichi Nagata, Akihiro Mizuno, Hideyuki Harada, Takayuki Ishikawa, Sachi Maeda, Fumiharu Ohka, Ryuji Yanase, Kogiku Shiba, Hironori Ueno, Kazuo Inaba, Ryuta Saito

{"title":"Dpcd Induces Hydrocephalus Because of Partial Defects in the Inner Dynein Arms, With Abnormal Ciliary Motility.","authors":"Taiki Yamamoto, Kazuhito Takeuchi, Yuichi Nagata, Akihiro Mizuno, Hideyuki Harada, Takayuki Ishikawa, Sachi Maeda, Fumiharu Ohka, Ryuji Yanase, Kogiku Shiba, Hironori Ueno, Kazuo Inaba, Ryuta Saito","doi":"10.1002/cm.70012","DOIUrl":"10.1002/cm.70012","url":null,"abstract":"Primary ciliary dyskinesia (PCD) is a congenital disease caused by gene mutations linked to ciliary dysfunction. PCD causes different symptoms, including chronic sinusitis, infertility, situs inversus and hydrocephalus. Motile cilia on ventricular ependymal cells are a crucial factor in cerebrospinal fluid circulation, and dysfunction of these cells causes hydrocephalus. Deleted in primary ciliary dyskinesia (Dpcd) is one genetic abnormality known to cause PCD, and its knockout leads to hydrocephalus in mice. PCD occurs in Dpcd -/- mice because of the lack of an inner dynein arm (IDA) in the motile cilia. However, how this deficiency is associated with the motility of ventricular ependymal motile cilia in Dpcd -/- mice has not been demonstrated. Herein, we show that Dpcd induces partial defects in dyneins and aberrant motility in ventricular ependymal cilia. In Dpcd -/- mice, the ependymal cilia demonstrated decreased amplitude, abnormal waveforms and low cerebrospinal fluid flow velocity. In addition, the amount of dynein axonemal heavy chains in some IDAs decreased in the ependymal cilia. In wild-type mice, Dpcd was localised in the cytoplasm and cilia of ependymal cells. Thus, abnormal ciliary movement in Dpcd -/- mice is likely attributed to a defect in IDA assembly in the ependymal cilia.","PeriodicalId":72766,"journal":{"name":"Cytoskeleton (Hoboken, N.J.)","volume":" ","pages":"237-249"},"PeriodicalIF":1.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735845","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

An Orthogonal Way of Writing the Tubulin Code. 编写微管蛋白代码的正交方法。

IF 1.6

Cytoskeleton (Hoboken, N.J.) Pub Date : 2026-05-01 Epub Date: 2025-06-28 DOI: 10.1002/cm.70002

Vicente Jose Planelles-Herrero, Emmanuel Derivery