Journal of cell science最新文献_第2页

Biphasic DNA damage and non-canonical replication stress response govern radiation-induced senescence in glioblastoma. 双相 DNA 损伤和非规范复制应激反应控制着胶质母细胞瘤的辐射诱导衰老。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-15 Epub Date: 2024-12-19 DOI: 10.1242/jcs.261844

Atanu Ghorai, Bhawna Singh, Shilpee Dutt

{"title":"Biphasic DNA damage and non-canonical replication stress response govern radiation-induced senescence in glioblastoma.","authors":"Atanu Ghorai, Bhawna Singh, Shilpee Dutt","doi":"10.1242/jcs.261844","DOIUrl":"10.1242/jcs.261844","url":null,"abstract":"Therapy-induced senescence (TIS) in glioblastoma (GBM) residual disease and escape from TIS account for resistance and recurrence, but the mechanism of TIS manifestation remains obscure. Here, we demonstrate that replication stress (RS) is critical for the induction of TIS in residual cells by employing an in vitro GBM therapy-resistance cellular model. Interestingly, we found a 'biphasic' mode of DNA damage after radiation treatment and reveal that the second phase of DNA damage arises majorly in the S phase of residual cells due to RS. Mechanistically, we show that persistent phosphorylated ATR is a safeguard for radiation resilience, whereas the other canonical RS molecules remain unaltered during the second phase of DNA damage. Importantly, RS preceded the induction of senescence, and ATR inhibition resulted in TIS reduction, leading to apoptosis. Moreover, ATR inhibition sensitized PARP-1 inhibitor-induced enhanced TIS-mediated resistance, leading to cell death. Our study demonstrates the crucial role of RS in TIS induction and maintenance in GBM residual cells, and targeting ATR alone or in combination with a PARP-1 inhibitor will be an effective strategy to eliminate TIS for better treatment outcomes.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

How to reduce your lab's carbon footprint. 如何减少实验室的碳足迹。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-15 Epub Date: 2024-12-16 DOI: 10.1242/jcs.263722

Julie Welburn

引用次数: 0

Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering. 变性肌肉和肌营养不良肌肉中 MiR-206 的调控及其对 AChR 聚类的影响

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-15 Epub Date: 2024-12-13 DOI: 10.1242/jcs.262303

Joseph Barden, Olivia Kosloski, Amir Jadidian, Mohammed Akaaboune

{"title":"Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering.","authors":"Joseph Barden, Olivia Kosloski, Amir Jadidian, Mohammed Akaaboune","doi":"10.1242/jcs.262303","DOIUrl":"10.1242/jcs.262303","url":null,"abstract":"The muscle-specific microRNA miR-206 has recently emerged as a potential regulator of genes involved in the formation and regeneration of the neuromuscular junction (NMJ). This study investigated miR-206-3p (miR-206) expression in synaptic and non-synaptic regions of denervated mice and α-dystrobrevin (Dtna)-knockout mice, as well as its impact on the formation and/or maintenance of agrin-induced acetylcholine receptor (AChR) clusters. In denervated, Dtna-deficient and crushed muscles, miR-206 expression significantly increased compared to what was seen for innervated muscles. Although miR-206 expression was slightly elevated in the synaptic regions of innervated muscles, it was dramatically increased in non-synaptic areas of denervated muscles. miR-206 targets transcripts of essential NMJ proteins, such as Dtna, α-syntrophin (Snta1) and rapsyn, but not the AChRα subunit (encoded by Chrna1) or Lrp4 in innervated muscles. However, in denervated muscles, AChRα transcripts, which increased significantly, become a target of miR-206. Co-expression of miR-206 with rapsyn, Dtna and Snta1 in C2C12 myoblasts significantly reduced their protein levels, and overexpression of miR-206 in myotubes disrupted agrin-induced AChR clustering. These results indicate that miR-206 fine-tunes NMJ signaling proteins by regulating transcripts of various proteins with different localizations under normal and pathological conditions.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Shear stress-stimulated AMPK couples endothelial cell mechanics, metabolism and vasodilation. 剪切应力刺激的 AMPK 将内皮细胞力学、新陈代谢和血管扩张联系在一起。

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-15 Epub Date: 2024-12-18 DOI: 10.1242/jcs.262232

Nicholas M Cronin, Logan W Dawson, Kris A DeMali

引用次数: 0

Phase separation of microtubule-binding proteins - implications for neuronal function and disease. 微管结合蛋白的相分离--对神经元功能和疾病的影响

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-15 Epub Date: 2024-12-13 DOI: 10.1242/jcs.263470

Daisy Duan, Anthony J Koleske

引用次数: 0

Altered calcium responses and antioxidant properties in Friedreich's ataxia-like cerebellar astrocytes.

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-09 DOI: 10.1242/jcs.263446

Chiara Marullo, Laura Croci, Iris Giupponi, Claudia Rivoletti, Sofia Zuffetti, Barbara Bettegazzi, Ottavio Cremona, Paola Giunti, Alessandro Ambrosi, Filippo Casoni, Gian Giacomo Consalez, Franca Codazzi

{"title":"Altered calcium responses and antioxidant properties in Friedreich's ataxia-like cerebellar astrocytes.","authors":"Chiara Marullo, Laura Croci, Iris Giupponi, Claudia Rivoletti, Sofia Zuffetti, Barbara Bettegazzi, Ottavio Cremona, Paola Giunti, Alessandro Ambrosi, Filippo Casoni, Gian Giacomo Consalez, Franca Codazzi","doi":"10.1242/jcs.263446","DOIUrl":"https://doi.org/10.1242/jcs.263446","url":null,"abstract":"Friedreich's ataxia (FRDA) is a neurodegenerative disorder characterized by severe neurological signs, affecting the peripheral and central nervous system, caused by reduced frataxin protein (FXN) levels. While several studies highlight cellular dysfunctions in neurons, there is limited information on the effects of FXN depletion in astrocytes and on the potential non-cell autonomous mechanisms affecting neurons in FRDA. In this study, we generated a model of FRDA cerebellar astrocytes to unveil phenotypic alterations that might contribute to cerebellar atrophy. We treated primary cerebellar astrocytes with an RNA interference-based approach, to achieve a reduction of FXN comparable to that observed in patients. These FRDA-like astrocytes display some typical features of the disease, such as an increase of oxidative stress and a depletion of glutathione content. Moreover, FRDA-like astrocytes exhibit decreased calcium responses to purinergic stimuli. Our findings shed light on cellular changes caused by FXN downregulation in cerebellar astrocytes, likely impairing their complex interaction with neurons. The potentially impaired ability to provide neuronal cells with glutathione or to release neuromodulators in a calcium-dependent manner could affect neuronal function, contributing to neurodegeneration.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142794777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stem cell expressed CXCR4 regulates tissue composition in the vomeronasal organ.

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-06 DOI: 10.1242/jcs.263451

André Dietz, Katja Senf, Eva M Neuhaus

{"title":"Stem cell expressed CXCR4 regulates tissue composition in the vomeronasal organ.","authors":"André Dietz, Katja Senf, Eva M Neuhaus","doi":"10.1242/jcs.263451","DOIUrl":"https://doi.org/10.1242/jcs.263451","url":null,"abstract":"The vomeronasal organ (VNO) detects signaling molecules that often prompt innate behaviors such as aggression and reproduction. Vomeronasal sensory neurons, classified into apical and basal lineages based on receptor expression, have a limited lifespan and are continuously replaced from a common stem cell niche. Using a combination of single-cell RNA sequencing data, immunofluorescence staining, and lineage tracing, we identified CXCR4 expression in proliferative stem cells and the basal neuronal lineage. Mice with a conditional knockout of Cxcr4 showed an increased number of SOX2-positive proliferative stem cells and enhanced basal neuronal lineage maturation. In addition, computational gene perturbation analysis revealed 87 transcription factors that may contribute to neurogenesis, among which SOX2. Conditional knockout of Cxcr4 did not only disturb neuronal maturation, but also affected non-neuronal cell types, resulting in a decrease of basal lamina lining quiescent stem cells and an increase in sustentacular support cells. Together, these findings enhance our understanding how a common pool of stem cells can give rise to different cell types of the VNO, highlighting the distinct role of CXCR4 in this process.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142785574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The co-chaperone DNAJA2 buffers proteasomal degradation of cytosolic proteins with missense mutations.

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-02 DOI: 10.1242/jcs.262019

Heather A Baker, Jonathan P Bernardini, Veronika Csizmók, Angel Madero, Shriya Kamat, Hailey Eng, Jessica Lacoste, Faith Au Yeung, Sophie Comyn, Elizabeth Hui, Gaetano Calabrese, Brian Raught, Mikko Taipale, Thibault Mayor

{"title":"The co-chaperone DNAJA2 buffers proteasomal degradation of cytosolic proteins with missense mutations.","authors":"Heather A Baker, Jonathan P Bernardini, Veronika Csizmók, Angel Madero, Shriya Kamat, Hailey Eng, Jessica Lacoste, Faith Au Yeung, Sophie Comyn, Elizabeth Hui, Gaetano Calabrese, Brian Raught, Mikko Taipale, Thibault Mayor","doi":"10.1242/jcs.262019","DOIUrl":"https://doi.org/10.1242/jcs.262019","url":null,"abstract":"Mutations can disrupt a protein's native function by causing misfolding, which is generally handled by an intricate protein quality control network. To better understand the triaging mechanisms of misfolded cytosolic proteins, we screened a human mutation library to identify a panel of unstable mutations. The degradation of these mutated cytosolic proteins is largely dependent on the ubiquitin proteasome system. Using BioID proximity labelling, we found that the co-chaperones DNAJA1 and DNAJA2 are key interactors with one of the mutated proteins. Notably, the absence of DNAJA2 increases the turnover of the mutant but not the wild-type protein. Our work indicates that specific missense mutations in cytosolic proteins can promote enhanced interactions with molecular chaperones. Assessment of the broader panel of cytosolic mutant proteins shows that the co-chaperone DNAJA2 exhibits two distinct behaviours: acting to stabilize a wide array of cytosolic proteins including wild type variants, and specifically \"buffer\" some mutant proteins to reduce their turnover. Our work illustrates how distinct elements of the protein homeostasis network are utilized in the presence of a cytosolic misfolded protein.","PeriodicalId":15227,"journal":{"name":"Journal of cell science","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Complexity and self-organization in the evolution of cell polarization.

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-01 Epub Date: 2024-12-11 DOI: 10.1242/jcs.263699

Marieke M Glazenburg, Liedewij Laan

引用次数: 0

Extracellular vesicles and nanoparticles at a glance.

IF 3.3 3区生物学

Journal of cell science Pub Date : 2024-12-01 Epub Date: 2024-12-06 DOI: 10.1242/jcs.260201

Dennis K Jeppesen, Qin Zhang, Robert J Coffey

引用次数: 0