Cell structure and function最新文献

Spatiotemporal regulation of microRNA-mediated gene silencing in cells. 细胞中microrna介导的基因沉默的时空调控。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-10-14 DOI: 10.1247/csf.26099

Aoi Satoh, Hayato Ito, Haruki Adachi, Hotaka Kobayashi

引用次数: 0

Cell-cycle-resolved τSTED nanoscopy reveals nanoscale reorganization of TGN46-positive structures. 细胞周期分辨τSTED纳米显微镜揭示了tgn46阳性结构的纳米级重组。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-10-08 Epub Date: 2026-09-12 DOI: 10.1247/csf.26065

Kaoru Katoh, Seigo Tateo, Toutai Mitsuyama, Koichi Kato

{"title":"Cell-cycle-resolved τSTED nanoscopy reveals nanoscale reorganization of TGN46-positive structures.","authors":"Kaoru Katoh, Seigo Tateo, Toutai Mitsuyama, Koichi Kato","doi":"10.1247/csf.26065","DOIUrl":"10.1247/csf.26065","url":null,"abstract":"The Golgi apparatus is a highly organized membrane system whose structure is remodeled during cell-cycle progression, but nanoscale changes in individual Golgi subdomains during interphase remain incompletely understood. Here, we used Fucci-compatible fluorescence lifetime-based STED (τSTED) nanoscopy to examine cell-cycle-associated reorganization of cis-Golgi and trans-Golgi network (TGN)-associated structures in fixed HeLa cells. By combining Fucci-SA reporters with red/far-red Golgi labeling, large-field sequential imaging, Abberior STAR RED nanobody labeling, and reproducible field-wise lifetime-trajectory-based τSTED reconstruction, we correlated Fucci-defined cell-cycle state with nanoscale Golgi morphology in individual cells. Automated morphometry showed that GM130-positive cis-Golgi and TGN46-positive trans/TGN-associated distribution domains were relatively compact in G1 cells, whereas TGN46-positive structures exhibited an expanded spatial distribution in G2-enriched cells. Optimized τSTED imaging resolved this expansion as dispersed submicron TGN46-positive structures rather than uniform enlargement of the Golgi apparatus. These findings reveal cell-cycle-associated spatial reorganization of TGN46-positive trans/TGN-associated structures and demonstrate the utility of cell-cycle-resolved super-resolution imaging for analyzing organelle architecture.Key words: Golgi apparatus, cell cycling, super-resolution microscopy, τSTED, Fucci.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"263-275"},"PeriodicalIF":1.8,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Tissue tension release induces Vinculin-dependent epithelial delamination in Drosophila pupal wings. 组织张力释放诱导蝇蛹羽部血管蛋白依赖的上皮分层。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-08-22 Epub Date: 2026-07-17 DOI: 10.1247/csf.26038

Souta Hiro, Keisuke Ikawa

{"title":"Tissue tension release induces Vinculin-dependent epithelial delamination in Drosophila pupal wings.","authors":"Souta Hiro, Keisuke Ikawa","doi":"10.1247/csf.26038","DOIUrl":"10.1247/csf.26038","url":null,"abstract":"Mechanical forces play critical roles in tissue morphogenesis and homeostasis, yet how tissue mechanics are translated into epithelial cell delamination remains poorly understood. Here, we use the Drosophila pupal wing as an in vivo model to examine how release of tissue tension influences cell death and delamination. Surgical severing of the wing hinge or loss of dumpy (dpy) function alters the force distribution, promotes cell crowding, and thereby significantly increases epithelial cell delamination compared to wild-type controls. An RNAi analysis targeting mechanosensitive components identified Vinculin, an adherens junction-associated force adaptor, as a key suppressor of mechanically induced cell delamination. Both tissue tension release and Vinculin depletion reduced junctional Vinculin levels and elevated Notch transcriptional activity, while canonical Notch transcriptional activation remained undetectable within delaminating cells. In contrast, knockdown of the Notch ligand Delta suppressed cell death and delamination. These findings indicate that release of tissue tension causes changes in forces acting on cells and cell crowding, thereby altering Vinculin-dependent regulation of Delta-Notch signaling and promoting cell delamination through a non-canonical Notch pathway.Key words: cell delamination, mechanotransduction, Delta-Notch pathways.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"249-262"},"PeriodicalIF":1.8,"publicationDate":"2026-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148535450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Jaw1 controls the granule abundance at a distinct ER compartment of pancreatic acinar cells. Jaw1控制胰腺腺泡细胞内不同ER区颗粒丰度。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-07-22 Epub Date: 2026-06-30 DOI: 10.1247/csf.26040

Hiroyuki Sato, Marielle Fernandez Bandalan, Kriengkamol Tantrakarn, Kenta Nakano, Tadashi Okamura, Yuki I Kawamura, Taeko Dohi, Takashi Tonozuka, Atsushi Nishikawa, Takuma Kozono

{"title":"Jaw1 controls the granule abundance at a distinct ER compartment of pancreatic acinar cells.","authors":"Hiroyuki Sato, Marielle Fernandez Bandalan, Kriengkamol Tantrakarn, Kenta Nakano, Tadashi Okamura, Yuki I Kawamura, Taeko Dohi, Takashi Tonozuka, Atsushi Nishikawa, Takuma Kozono","doi":"10.1247/csf.26040","DOIUrl":"10.1247/csf.26040","url":null,"abstract":"Pancreatic acinar cells (PACs) are specialized for the production and secretion of digestive enzymes. PACs are highly polarized, with rough endoplasmic reticulum (ER) located in the basal and lateral regions, while zymogen granules (ZG) are localized apically. Furthermore, a distinct ER compartment containing inositol 1,4,5-trisphosphate receptors (IP3Rs), which are Ca2+ channels, is positioned underneath the filamentous-actin and tight junctions in the apical region. This structurally polarized architecture underlies the localized elevation of Ca2+ levels in the apical region, which supports the efficient secretion of granules. In this report, we show that Jaw1, a regulatory protein of IP3Rs, is a new component of the distinct ER compartment in PACs, colocalizing with IP3R2 and IP3R3 rather than IP3R1. Importantly, PACs from Jaw1-deficient mice exhibited an accumulation of ZG and cell hypertrophy without disrupting both the arrangement of the distinct ER compartment and the localization of IP3Rs. These findings shed more light on the underlying molecular components of the distinct ER compartment in the apical region of PACs, offering insights into their physiological functions in the homeostatic control of ZG abundance in PACs.Key words: cell polarity, ER, IP3Rs, Jaw1, pancreatic acinar cells.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"237-248"},"PeriodicalIF":1.8,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

CCL5 enhances invasion of squamous cell carcinoma via syndecan-1-dependent ERK signaling. CCL5通过syndecan-1依赖性ERK信号增强鳞状细胞癌的侵袭。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-06-20 Epub Date: 2026-05-19 DOI: 10.1247/csf.26030

Toko Yamazaki, Yuji Kumagai, Kosuke Maeda, Tomoyasu Aizawa, Kosuke Maekawa, Atsushi Enomoto, Seiichiro Ishihara, Hisashi Haga

{"title":"CCL5 enhances invasion of squamous cell carcinoma via syndecan-1-dependent ERK signaling.","authors":"Toko Yamazaki, Yuji Kumagai, Kosuke Maeda, Tomoyasu Aizawa, Kosuke Maekawa, Atsushi Enomoto, Seiichiro Ishihara, Hisashi Haga","doi":"10.1247/csf.26030","DOIUrl":"10.1247/csf.26030","url":null,"abstract":"Cancer cells form clusters and invade the surrounding stroma. This phenomenon is associated with metastasis and poor prognosis in patients with cancer. Therefore, prevention of invasion may improve cancer therapy. A previous study suggested that the C-C motif chemokine ligand 5 (CCL5) is more highly expressed in the highly invasive subclone than in the less invasive subclone derived from A431 cell line, a model of human skin squamous cell carcinoma. However, the role of CCL5 and the mechanisms through which it regulates invasion in A431 cell clusters remain unclear. Herein, we investigated the molecular mechanisms underlying CCL5-induced invasion in A431 cell clusters. Knockdown of CCL5 suppressed invasion on A431 cell clusters, whereas treatment with recombinant CCL5 promoted invasion of them. Mechanistically, CCL5 increased the phosphorylation levels of Src and ERK, leading to the invasion of A431 cell clusters. Furthermore, the knockdown of syndecan-1 (SDC1), a transmembrane protein known to interact to CCL5, suppressed CCL5-induced invasion in A431 cell clusters. Consistently, knockdown of SDC1 reduced the level of phosphorylated ERK. These findings demonstrate that the CCL5 promotes the invasion of A431 cells clusters through SDC1-dependent ERK signaling and Src phosphorylation.Key words: invasion, CCL5, syndecan-1, ERK signaling, Src.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"227-235"},"PeriodicalIF":1.8,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147980546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Metformin attenuates cuprizone-induced mitochondrial dysfunction and senescence-associated changes in primary neuronal cells. 二甲双胍减轻铜酮诱导的线粒体功能障碍和原代神经元细胞衰老相关的变化。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-06-20 Epub Date: 2026-05-21 DOI: 10.1247/csf.26019

Yeojin Kim, Hyunbum Jeon, Sun-Yeong Gwon, Sehyun Chae, Ji Young Mun

{"title":"Metformin attenuates cuprizone-induced mitochondrial dysfunction and senescence-associated changes in primary neuronal cells.","authors":"Yeojin Kim, Hyunbum Jeon, Sun-Yeong Gwon, Sehyun Chae, Ji Young Mun","doi":"10.1247/csf.26019","DOIUrl":"10.1247/csf.26019","url":null,"abstract":"Mitochondrial dysfunction and cellular senescence are key features of brain aging and neurodegenerative diseases. Cuprizone (CPZ), a mitochondrial toxin, induces oxidative stress, abnormal lipid metabolism, and iron accumulation in neurons and oligodendrocytes. Here, we investigated whether metformin (MFN), an AMPK activator with a known safety profile, can protect against CPZ-induced mitochondrial and senescence-like changes. Using confocal and transmission electron microscopy, we observed mitochondrial enlargement, increased reactive oxygen species (ROS) production, iron accumulation, and lipofuscin formation in CPZ-treated primary neuronal cultures. Next, we assessed the impact of MFN on mitochondrial changes and increase in lipid-radicals in cells exposed to CPZ. The treatment of MFN resulted in decreased abnormal mega-mitochondrial morphology, decreased levels of mitochondrial reactive oxygen species (mitoROS), and decreased iron accumulation within mitochondria. Moreover, MFN treatment prevented the typically observed increases in lipofuscin and lipid radicals in CPZ-affected cells. Analysis of gene expression in primary neuronal cells treated with CPZ showed differences in mitochondria-related genes linked to lipid peroxidation, oxidative stress, and cellular senescence. These findings suggest that MFN mitigates mitochondrial dysfunction and senescence-associated alterations, highlighting its therapeutic potential in aging-related neurodegeneration.Key words: mitochondria, CPZ, MFN, oxidative stress, lipofuscin.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"215-226"},"PeriodicalIF":1.8,"publicationDate":"2026-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147962572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Loss of macroautophagy results in abnormality of the endoplasmic reticulum in insulin-secreting MIN6 cells. 巨噬丧失导致胰岛素分泌MIN6细胞内质网异常。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-06-10 Epub Date: 2026-05-09 DOI: 10.1247/csf.26016

Asako Kishimoto, Shunsuke Saito, Byungseok Jin, Shigeomi Shimizu, Satoko Arakawa, Kazutoshi Mori

{"title":"Loss of macroautophagy results in abnormality of the endoplasmic reticulum in insulin-secreting MIN6 cells.","authors":"Asako Kishimoto, Shunsuke Saito, Byungseok Jin, Shigeomi Shimizu, Satoko Arakawa, Kazutoshi Mori","doi":"10.1247/csf.26016","DOIUrl":"10.1247/csf.26016","url":null,"abstract":"Macroautophagy is a highly conserved system that degrades various materials inside the cell ranging from proteins to organelles. Atg5 is a protein essential for the formation of autophagosomes, which sequester materials by double membrane and degrade them after fusion with lysosomes. MIN6 cells derived from mouse pancreatic β cells retain the ability to secrete insulin in response to a change in glucose concentration from low to high. We knocked out the Atg5 gene in MIN6 cells and identified an abnormality in the endoplasmic reticulum (ER) under normal culture conditions using electron microscopy. The ER was slightly enlarged and the ER membrane was ruptured at some places adjacent to inclusion body-like structures. Numerous granule-like structures were accumulated in the lumen of the ER, some of which appeared to have leaked into the cytoplasm. These abnormalities caused ER stress, resulting in activation of all three pathways (IRE1, PERK, and ATF6) of the unfolded protein response but no induction of apoptosis. We also observed the activation of alternative autophagy/Golgi membrane-associated degradation in Atg5-KO MIN6 cells, but this was insufficient for the removal of a majority of these granule-like structures from the ER. Thus, macroautophagy but not activation of the unfolded protein response or Golgi membrane-associated degradation is essential for the homeostasis of the ER in MIN6 cells.Key words: autophagy, endoplasmic reticulum, unfolded protein response, proinsulin, Golgi membrane-associated degradation.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"203-213"},"PeriodicalIF":1.8,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147866934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Changes in nuclear morphology and size in mammalian temperature-sensitive mutants. 哺乳动物温度敏感突变体核形态和大小的变化。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-04-11 Epub Date: 2026-03-14 DOI: 10.1247/csf.26002

Kimihiko Sugaya

引用次数: 0

Identification of Rab30 as a novel regulator of tubular endosomes. Rab30作为管状核内体新调控因子的鉴定。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-04-11 Epub Date: 2026-03-14 DOI: 10.1247/csf.25161

Shumpei Nakashima, Mitsunori Fukuda

{"title":"Identification of Rab30 as a novel regulator of tubular endosomes.","authors":"Shumpei Nakashima, Mitsunori Fukuda","doi":"10.1247/csf.25161","DOIUrl":"10.1247/csf.25161","url":null,"abstract":"Tubular-shaped recycling endosomes, known as tubular endosomes, are present in certain types of cells, including HeLa cells, and they regulate the recycling of clathrin-independent endocytosed (CIE) cargo proteins to the plasma membrane. Several key regulators of tubular endosomes, including Rab small GTPases and related proteins, have been identified thus far, but the entire process of tubular endosome formation is not yet fully understood. We previously showed that expression of a Golgi-related Rab-GTPase-activating protein TBC1D22B in HeLa cells caused their tubular structures to disappear, suggesting a possible link between tubular endosome formation and a certain Golgi function(s). However, nothing is known about the target Rab(s) of TBC1D22B in tubular endosome formation or about the functional relationship between tubular endosomes and the Golgi apparatus. Here, we performed comprehensive Rab-knockdown screening in combination with dominant-negative Rab expression and succeeded in identifying 12 Rabs as regulators of tubular endosome formation. One of them, Rab30, a Golgi-resident Rab, is a novel target of TBC1D22B and involved in both tubular endosome formation and CIE cargo trafficking. We also showed that a Rab30-BICD2-KIF5B axis is likely to be involved in tubular endosome formation. Our findings suggest the importance of Rab30-mediated post-Golgi trafficking in tubular endosome formation.Key words: Golgi, GTPase-activating protein (GAP), Rab30, siRNA screening, tubular endosome.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"177-189"},"PeriodicalIF":1.8,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147462740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Functional analysis of miR-199a-3p in tumor endothelial cells. miR-199a-3p在肿瘤内皮细胞中的功能分析。

IF 1.8 4区生物学

Cell structure and function Pub Date : 2026-04-01 Epub Date: 2026-02-25 DOI: 10.1247/csf.25167

Yuying Hong, Li Yu, Ikuko Takahashi, Nako Maishi, Aya Matsuda, Yuya Sakurai, Yasuhiro Hida, Ikuya Miyamoto, Kyoko Hida

{"title":"Functional analysis of miR-199a-3p in tumor endothelial cells.","authors":"Yuying Hong, Li Yu, Ikuko Takahashi, Nako Maishi, Aya Matsuda, Yuya Sakurai, Yasuhiro Hida, Ikuya Miyamoto, Kyoko Hida","doi":"10.1247/csf.25167","DOIUrl":"10.1247/csf.25167","url":null,"abstract":"Tumor endothelial cells (TECs) play a key role in tumor growth and metastasis. They exhibit distinct phenotypic and functional features compared with normal endothelial cells (NECs). Although microRNAs (miRNAs) play diverse roles in tumor progression, the differences in the miRNA expression profiles between TECs and NECs and their role in the TEC phenotype remain unclear.In this study, we isolated NECs and TECs from non-tumor and tumor regions of human renal cancer tissues and conducted an miRNA array analysis. Of the 13 differentially expressed miRNAs, miR-199a-3p was expressed the highest in TECs. Overexpression of miR-199a-3p in NECs significantly enhanced their proliferation, migration, and invasion.Target gene analysis using four databases identified CD151 as a potential target of miR-199a-3p. CD151 expression was downregulated in TECs compared with NECs, and miR-199a-3p transfection decreased CD151 expression in NECs. CD151 knockdown by siRNA promotes cell proliferation, migration, and invasion, and reduces cell adhesion to the extracellular matrix. Moreover, miR-199a-3p overexpression and CD151 silencing upregulated MMP2 expression in TECs. Taken together, these results suggest that miR-199a-3p contributes to the proangiogenic phenotype in TECs by suppressing CD151 expression.Key words: miR-199a-3p, tumor endothelial cells, CD151, angiogenesis, cell migration and invasion.","PeriodicalId":9927,"journal":{"name":"Cell structure and function","volume":" ","pages":"163-176"},"PeriodicalIF":1.8,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147303041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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