Genes to Cells最新文献

Nuclear Wrinkles Result From Geometric Adaptations to Cellular and Nuclear Morphological Changes in Epithelial Cells 细胞核皱纹是上皮细胞对细胞和细胞核形态变化的几何适应的结果。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-10-09 DOI: 10.1111/gtc.70152

Le Minh Khoa, Yohei Kono, Takeshi Shimi, Hiroshi Kimura

{"title":"Nuclear Wrinkles Result From Geometric Adaptations to Cellular and Nuclear Morphological Changes in Epithelial Cells","authors":"Le Minh Khoa, Yohei Kono, Takeshi Shimi, Hiroshi Kimura","doi":"10.1111/gtc.70152","DOIUrl":"10.1111/gtc.70152","url":null,"abstract":"Mechanical cues influence cell behavior and fate and are frequently accompanied by changes in nuclear shape; however, how epithelial nuclei accommodate such deformations remains incompletely understood. In this article, we investigated the formation and regulation of nuclear wrinkles (NWs), inward folds of the nuclear envelope, in human epithelial cells. Using quantitative confocal imaging in 2.5D spheroid cultures and controlled 2D monolayers, we found that NWs formed frequently in MCF10A cells but rarely in hTERT-RPE1 cells, indicating pronounced cell-type specificity. NW frequency increased with cell density and was tightly associated with coordinated geometric changes consistent with nuclear rounding. Disruption of F-actin organization, but not microtubules, robustly induced NW formation, and acute cell rounding triggered by trypsinization was sufficient to induce widespread wrinkling across multiple cell types. Live-cell imaging revealed that NWs are dynamic and reversible at low cell density but become stabilized under sustained confinement. NW formation occurred without detectable nuclear envelope rupture, DNA damage, or stress-associated histone phosphorylation. Quantitative analysis supports a passive geometric model in which redistribution of excess nuclear surface area accommodates nuclear shape remodeling, allowing epithelial nuclei to buffer mechanical constraints while preserving nuclear integrity.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70152","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149140363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-Invasive Visualization of Cells Expressing Unmodified Target mRNA Using a Programmable RNA-Mediated BiFC Platform 使用可编程rna介导的BiFC平台对表达未修饰靶mRNA的细胞进行无创可视化

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-10-07 DOI: 10.1111/gtc.70151

Naoki Yamamoto, Sayaka Takase-Yoden

引用次数: 0

A YAP–TEAD–CTCF Transcriptional Regulatory Axis Associated With the Elimination of Injured Hepatocytes From the Liver YAP-TEAD-CTCF转录调控轴与肝脏损伤肝细胞的清除有关

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-10-04 DOI: 10.1111/gtc.70150

Daiki Hatakeyama, Yoshimi Okamoto-Uchida, Misaki Kosaka, Haruka Hirose, Satoshi Kofuji, Keiko Danzaki, Yoshiki Endo, Michiko Nakagawa, Akinori Kanai, Yutaka Suzuki, Takeshi Yokoo, Shuji Terai, Teppei Shimamura, Hiroshi Nishina

{"title":"A YAP–TEAD–CTCF Transcriptional Regulatory Axis Associated With the Elimination of Injured Hepatocytes From the Liver","authors":"Daiki Hatakeyama, Yoshimi Okamoto-Uchida, Misaki Kosaka, Haruka Hirose, Satoshi Kofuji, Keiko Danzaki, Yoshiki Endo, Michiko Nakagawa, Akinori Kanai, Yutaka Suzuki, Takeshi Yokoo, Shuji Terai, Teppei Shimamura, Hiroshi Nishina","doi":"10.1111/gtc.70150","DOIUrl":"https://doi.org/10.1111/gtc.70150","url":null,"abstract":"The liver maintains tissue homeostasis both by undergoing regeneration and by eliminating abnormal or injured hepatocytes. The transcriptional coactivator YAP in collaboration with the TEAD family of transcription factors regulates hepatocyte proliferation. It has also been associated with injured hepatocyte elimination whereby YAP-active injured hepatocytes are extruded into the sinusoidal lumen and undergo cell death followed by macrophage phagocytosis. However, the molecular mechanisms underlying this process are unknown. To address this, we performed RNA-seq analysis in YAP-active injured hepatocytes that are eliminated from the liver. We found increased expression of multiple genes associated with cell cycle arrest and cytoskeletal remodeling. Ligand–receptor analysis using single-cell spatial transcriptomics showed that YAP-active hepatocytes express the secreted factors CSF1 and CCL2, which promote macrophage recruitment and activation. ATAC-seq analysis in YAP-active hepatocytes revealed a significant increase in chromatin accessibility at regions containing CTCF-binding motifs, and the YAP–TEAD4 complex associated with CTCF in the nucleus. These results indicate that a YAP–TEAD–CTCF axis shapes the gene expression program underlying injured hepatocyte elimination through chromatin structural remodeling, resulting in liver homeostasis.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dishevelled2 Negatively Regulates Cell-Surface Ror1 Abundance Through Lysosomal Degradation Dishevelled2通过溶酶体降解负调控细胞表面Ror1丰度

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-10-03 DOI: 10.1111/gtc.70153

Rie Zenda, Kyoka Hoshi, Koki Kamizaki, Yasuhiro Minami, Ken Iseki, Michiru Nishita

{"title":"Dishevelled2 Negatively Regulates Cell-Surface Ror1 Abundance Through Lysosomal Degradation","authors":"Rie Zenda, Kyoka Hoshi, Koki Kamizaki, Yasuhiro Minami, Ken Iseki, Michiru Nishita","doi":"10.1111/gtc.70153","DOIUrl":"https://doi.org/10.1111/gtc.70153","url":null,"abstract":"<div>\u0000 \u0000 Receptor tyrosine kinase-like orphan receptor 1 (Ror1) mediates Wnt5a-dependent noncanonical Wnt signaling and promotes lung adenocarcinoma progression. Dishevelled (Dvl) proteins are central mediators of Wnt signaling and have also been implicated in its negative regulation and receptor turnover. However, whether Dvl2 contributes to negative regulation of Wnt5a–Ror1 signaling remains unclear. Here, we show that Dvl2 depletion selectively increased the cell surface-associated 130-kDa Ror1 species without affecting Ror1 mRNA levels. Wnt5a depletion similarly increased Ror1 abundance, which was reverted by an addition of recombinant Wnt5a. Dvl2 promoted degradation of the 130-kDa Ror1 species through a lysosomal rather than proteasomal pathway, and CK1 inhibition stabilized the receptor. Dvl2 interacted with the intracellular C-terminal region of Ror1 via its DEP domain, and CK1 inhibition enhanced this interaction. Furthermore, both the intracellular C-terminal region and extracellular cysteine-rich domain of Ror1 were required for Dvl2-mediated receptor destabilization. These findings reveal a previously unrecognized role for Dvl2 in regulating Ror1 turnover and suggest that Dvl2-mediated lysosomal degradation of Ror1 may provide a negative-feedback mechanism that limits Wnt5a–Ror1 signaling.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099900","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

Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis 奈兰司特与肺泡上皮细胞状态动力学改变有关，同时减弱肺纤维化的纤维化重塑

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-10-03 DOI: 10.1111/gtc.70149

Nanako Hamada, Yoshiaki Hayashi, Daisuke Motooka, Atsushi Kuwahara, Shizuo Akira, Kiyoharu Fukushima

{"title":"Nerandomilast is Associated With Altered Alveolar Epithelial Cell State Dynamics While Attenuating Fibrotic Remodeling in Pulmonary Fibrosis","authors":"Nanako Hamada, Yoshiaki Hayashi, Daisuke Motooka, Atsushi Kuwahara, Shizuo Akira, Kiyoharu Fukushima","doi":"10.1111/gtc.70149","DOIUrl":"https://doi.org/10.1111/gtc.70149","url":null,"abstract":"Pulmonary fibrosis is a progressive and life-threatening lung disorder characterized by excessive fibrogenesis and impaired respiratory function. Nerandomilast, a preferential phosphodiesterase 4B inhibitor, is currently approved for the treatment of idiopathic pulmonary fibrosis and progressive pulmonary fibrosis in several countries following its demonstrated clinical efficacy in Phase III trials. However, its cellular mechanisms of action remain incompletely understood. In this study, we investigated the effects of nerandomilast on a bleomycin-induced mouse model of lung fibrosis. Nerandomilast treatment attenuates fibrotic remodeling and preserves alveolar epithelial architecture. Single-cell transcriptomic analyses revealed altered alveolar epithelial cell state dynamics accompanied by increased cell cycle-associated pathways in alveolar type 2 cells and an increased relative abundance of alveolar type 2 cells. Consistent with the single-cell findings, nerandomilast was associated with an increased SFTPC-positive area and the preservation of alveolar epithelial architecture in vivo. Collectively, our findings suggest that nerandomilast attenuates fibrotic remodeling while modulating alveolar epithelial cell state dynamics, which may provide a possible cellular explanation for its clinical efficacy in patients with pulmonary fibrosis.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 6","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70149","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149099899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The HMG-CoA Reductase Inhibitor Fluvastatin Promotes Th2-Skewed Immune Responses by Modulating Dendritic Cell Differentiation HMG-CoA还原酶抑制剂氟伐他汀通过调节树突状细胞分化促进th2偏斜免疫反应。

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-09-01 DOI: 10.1111/gtc.70148

Satoshi Ishikawa, Haruka Mizuno, Kanon Murase, Kazuki Sasano, Isamu Ogawa, Yuka Itoh, Saotomo Itoh, Shigeaki Hida

{"title":"The HMG-CoA Reductase Inhibitor Fluvastatin Promotes Th2-Skewed Immune Responses by Modulating Dendritic Cell Differentiation","authors":"Satoshi Ishikawa, Haruka Mizuno, Kanon Murase, Kazuki Sasano, Isamu Ogawa, Yuka Itoh, Saotomo Itoh, Shigeaki Hida","doi":"10.1111/gtc.70148","DOIUrl":"10.1111/gtc.70148","url":null,"abstract":"Statins, inhibitors of HMG-CoA reductase, exert immunomodulatory effects beyond lipid lowering, yet how they regulate T helper (Th) cell differentiation remains poorly understood. We show that fluvastatin administration to C57BL/6 mice for 7 days suppressed interferon-γ and elevated interleukin-4 production by splenic CD4+ T cells, shifting the immune balance toward Th2 without altering splenocyte numbers or major immune cell subset proportions. This effect was not shared by rosuvastatin, suggesting that lipophilicity-dependent cellular uptake influences immunomodulatory potency. In vitro experiments confirmed a direct Th2-promoting action of fluvastatin on CD4+ T cells. Basophils were excluded as mediating cells, as fluvastatin suppressed rather than enhanced basophil interleukin-4 production. Continuous fluvastatin exposure during granulocyte-macrophage colony-stimulating factor (GM-CSF)-driven dendritic cell (DC) differentiation altered the phenotype of the resulting DCs and markedly enhanced their Th2-polarizing capacity in co-cultures with antigen-specific CD4+ T cells. These functional changes were accompanied by alterations in DC surface molecule expression, although their causal contribution remains to be established. These findings indicate that continuous fluvastatin exposure during DC differentiation is associated with an altered DC phenotype and enhanced Th2-polarizing capacity.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13533597/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148877238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Signal Transducing Adaptor Protein-2 Represses Epithelial-Mesenchymal Transition by Downregulating SMAD-Mediated ZEB1 Expression 信号转导接头蛋白2通过下调smad介导的ZEB1表达抑制上皮-间质转化

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-28 DOI: 10.1111/gtc.70147

Fumiya Okuyama, Yuichi Kitai, Zhengcheng Li, Mikito Ishii, Ryuta Muromoto, Tadashi Matsuda

引用次数: 0

Transforming Life Science Through Chromosome-Level Genome Assemblies 通过染色体水平的基因组组装改变生命科学

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-21 DOI: 10.1111/gtc.70145

Tetsuo Kon, Kosuke Kataoka, Yi-Jyun Luo, Johannes Nicolaus Wibisana, Kouhei Toga, Narumi Uno, Yuki Monden, Mayuko Hamada

{"title":"Transforming Life Science Through Chromosome-Level Genome Assemblies","authors":"Tetsuo Kon, Kosuke Kataoka, Yi-Jyun Luo, Johannes Nicolaus Wibisana, Kouhei Toga, Narumi Uno, Yuki Monden, Mayuko Hamada","doi":"10.1111/gtc.70145","DOIUrl":"https://doi.org/10.1111/gtc.70145","url":null,"abstract":"Advances in long-read sequencing and Hi–C scaffolding have made chromosome-level genome assembly increasingly accessible to individual laboratories, shifting genome research from large consortium-led projects toward investigator-driven studies across diverse taxa. This transition allows researchers to select organisms based on biological questions rather than the prior availability of genomic resources. In this review, we summarize the core experimental and computational steps for generating, evaluating, and annotating chromosome-level assemblies, and examine how they have advanced research in non-model organisms and genetically complex systems. Representative case studies illustrate four major contributions: resolving structural variation and lineage-specific genome architecture, linking genome organization to phenotypic innovation and plasticity, reconstructing deep chromosome evolution and macrosynteny, and distinguishing homologous and homoeologous chromosomes in polyploid genomes. These examples show that chromosome-level assemblies provide more than complete reference sequences. They establish a continuous genomic coordinate system through which genes, regulatory elements, transposable element insertions, sequence variants, and cellular states can be interpreted within broader chromosomal, population, and evolutionary contexts. We describe this integrative perspective as “glocal biology.” Future progress will require pangenomic, population-scale, and haplotype-resolved resources integrated with multi-omics and functional analyses. Collectively, chromosome-level genomics is reshaping life science by embedding molecular functions within chromosomal and evolutionary contexts.","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/gtc.70145","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148785072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The First International Workshop on Cell Division Cycles at OIST OIST第一届细胞分裂周期国际研讨会

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-19 DOI: 10.1111/gtc.70146

Yang Ming, Yutei Takahashi, Aurellia Ramara Winaya, Tolkyn Seterkhan, Tomomi Kiyomitsu

{"title":"The First International Workshop on Cell Division Cycles at OIST","authors":"Yang Ming, Yutei Takahashi, Aurellia Ramara Winaya, Tolkyn Seterkhan, Tomomi Kiyomitsu","doi":"10.1111/gtc.70146","DOIUrl":"https://doi.org/10.1111/gtc.70146","url":null,"abstract":"<div>\u0000 \u0000 Small-scale recurring international workshops dedicated to the cell cycle have become well established in Europe and the United States, but not in Japan. To establish such a workshop in Japan, four principal investigators at the Okinawa Institute of Science and Technology Graduate University (OIST) organized the First International Workshop on Cell Division Cycles, entitled “Emerging Concepts in Cell Division Cycles 2026—From Early Development to Cancer and Aging,” in Okinawa, Japan, from March 2 to 5, 2026. The meeting brought together 17 world-leading experts and a total of 74 participants from diverse fields spanning cell division, cancer, and aging. The speakers presented cutting-edge studies employing a wide range of advanced approaches, including large-scale translational isoform analyses, new experimental systems and model organisms, ultrastructure expansion microscopy, and anti-aging strategies. These advances highlighted recent progress in understanding the mechanisms that ensure faithful genome inheritance and their relevance to development, disease, and evolution. Here, we summarize the 36 oral presentations, together with photographs from the workshop, and share our reflections and perspectives with the community in the hope that the OIST Cell Division Workshop will continue to grow as a recurring international forum for cell division and cell cycle research.\u0000 </div>","PeriodicalId":12742,"journal":{"name":"Genes to Cells","volume":"31 5","pages":""},"PeriodicalIF":1.4,"publicationDate":"2026-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148784403","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

Identification of the Down Syndrome Critical Region 3 Gene as a Mammalian Cell Size Regulator 唐氏综合征关键区3基因作为哺乳动物细胞大小调节因子的鉴定

IF 1.4 4区生物学

Genes to Cells Pub Date : 2026-08-14 DOI: 10.1111/gtc.70142

Kazumi Kimura, Masakazu Souda, Ryotaro Mori, Yoshimi Kato, Hiroki Kurahashi, Masashi Asai, Kazuo Yamamoto

引用次数: 0