{"title":"Piezo mediates oviposition in shielding gaps to protect moth eggs from parasitoid wasp.","authors":"Baiwei Ma, Dong Ai, Liwei Zhang, Hanbo Zhao, Jiayu Wang, Xiaolan Liu, Guirong Wang","doi":"10.1016/j.celrep.2025.116035","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.116035","url":null,"abstract":"<p><p>Where to lay eggs is critical for insect females to avoid risks and ensure offspring survival. Females of the oriental armyworm, Mythimna separata, deposit their eggs inside narrow slits to evade predators. However, the sensory mechanism by which they choose the optimal slit for egg laying remains unclear. Here, we demonstrate the requirement of mechanosensation for selecting oviposition slit. Females preferentially deposit eggs in the leaf sheath or in folded paper gaps, thereby shielding their eggs from parasitism by Trichogramma dendrolimi. Specifically, females prefer the opening of 0.5 mm in rigid gaps. Surgical ablation of ovipositor bristles leads to disrupted gap selection and increased parasitism. Mechanosensitive receptor Piezo is found within these bristles and responds to the mechanical deflection of a single bristle. Piezo mutants show random egg laying and vulnerability to parasitoids. Collectively, our findings provide insight into the involvement of mechanosensation in insect egg-laying site choice.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 8","pages":"116035"},"PeriodicalIF":7.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-23DOI: 10.1016/j.celrep.2025.116018
Ran Zhang, Weiwei Yan, Jupeng Yuan, Yuequn Ma, Ziyuan Ren, Xi Chen, Juncai Lv, Meng Wu, Jinming Yu, Dawei Chen
{"title":"Cancer-associated fibroblast-derived fibulin-5 promotes radioresistance in non-small-cell lung cancer.","authors":"Ran Zhang, Weiwei Yan, Jupeng Yuan, Yuequn Ma, Ziyuan Ren, Xi Chen, Juncai Lv, Meng Wu, Jinming Yu, Dawei Chen","doi":"10.1016/j.celrep.2025.116018","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.116018","url":null,"abstract":"<p><p>Radioresistance impedes the effectiveness of cancer radiotherapy, particularly due to the persistence of cancer-associated fibroblasts (CAFs) post-radiation. This study aims to identify CAF-expressed molecules predicting radiotherapy efficacy and to clarify the resistance mechanisms in non-small-cell lung cancer (NSCLC). We identified higher Fibulin-5 (FBLN5) expression in the stromal regions of recurrent patients after radiotherapy utilizing spatial transcriptomics and FBLN5 knockdown in CAFs enhanced radiosensitivity. Mechanistically, Fibulin-5 binds to integrin αVβ5 receptor, activates the Src-STAT3 pathway in CAFs and cancer cells, downregulates acyl-CoA synthetase long-chain family member 4 (ACSL4), and impairs irradiation-activated ferroptosis. Radioresistant cancer cells are more capable of converting normal fibroblasts to CAFs, upregulating FBLN5 via exosomal miRNA. Activated CAFs further promote tumor radioresistance, confirmed by single-cell RNA sequencing. Clinical tissue analysis showed that elevated Fibulin-5 expression is correlated with fibroblast activation and radioresistance. Thus, high Fibulin-5 expression in CAFs serves as a predictive biomarker for radiotherapy efficacy and a potential therapeutic target to improve NSCLC radiosensitivity.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 8","pages":"116018"},"PeriodicalIF":7.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144715056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-23DOI: 10.1016/j.celrep.2025.116019
Yoon Ki Joo, Carlos Ramirez Parrado, Wenxue Li, Ran Yang, Elizabeth Black, Franziska Bleichert, Yansheng Liu, Lilian Kabeche
{"title":"The mitotic ATR-Chk1 pathway promotes CDK1 activity for faithful chromosome segregation.","authors":"Yoon Ki Joo, Carlos Ramirez Parrado, Wenxue Li, Ran Yang, Elizabeth Black, Franziska Bleichert, Yansheng Liu, Lilian Kabeche","doi":"10.1016/j.celrep.2025.116019","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.116019","url":null,"abstract":"<p><p>Ataxia telangiectasia and Rad3-related (ATR) and checkpoint kinase 1 (Chk1) are crucial kinases in the DNA damage response (DDR) pathway. While the roles of ATR and Chk1 within the DDR are well established, their roles in mitosis are not fully understood. Here, we describe that the ATR-Chk1 pathway is rewired during mitosis to promote full CDK1 activity, starkly contrasting its role in interphase, where it inhibits CDK1 following DNA damage in human cells. In mitosis, Chk1 inhibits residual activity of PKMYT1 (Myt1) via direct phosphorylation at Serine 143. Partial loss of CDK1 activity caused by inhibition of mitotic Chk1 leads to different effects on mitotic progression than full CDK1 inhibition. It causes increased lagging chromosomes in part through loss of Aurora B activity. Thus, mitosis-specific ATR-Chk1 activity is necessary to promote faithful chromosome segregation by ensuring that CDK1 activity is maintained in mitosis.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 8","pages":"116019"},"PeriodicalIF":7.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cell-of-origin-specific behavioral deficits in oligodendrocyte-derived glioblastoma.","authors":"Divsha Sher, Ignacio Mastandrea, Alina Brosque, Gilad Levy, Itamar Ironi, Guy Shapira, Noam Shomron, Boaz Barak, Dinorah Friedmann-Morvinski","doi":"10.1016/j.celrep.2025.116043","DOIUrl":"https://doi.org/10.1016/j.celrep.2025.116043","url":null,"abstract":"<p><p>Glioblastoma (GBM) remains the most lethal primary brain tumor, persisting despite multimodal standard-of-care therapy. One of the major challenges for effective treatment of these tumors is their high heterogeneity, which stems, in part, from differences in the cell of origin. Using a CNP-Cre transgenic mouse model, this study investigates the role of differentiated oligodendrocytes as a candidate cell of origin for GBM. We show that these cells can give rise to GBM tumors when targeted with Cre-inducible oncogenic lentiviral vectors. Notably, in mice these oligodendrocyte-derived GBM tumors lead to early-onset motor deficits that are not observed in neuron-derived tumors. In addition, these tumors exhibit a distinct transcriptional profile involving altered expression of myelin-related genes, emphasizing the impact of the cell of origin on both molecular and behavioral phenotypes of GBM. We believe that a deeper understanding of the identity of the cell of origin may contribute to uncovering new mechanisms and therapeutic vulnerabilities in GBM.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 8","pages":"116043"},"PeriodicalIF":7.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144706501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-22Epub Date: 2025-06-18DOI: 10.1016/j.celrep.2025.115878
Chinenye L Ekemezie, Lewis I Chan, Charlotte R Brown, Karla Helena-Bueno, Tom A Williams, Sergey V Melnikov
{"title":"Extensive natural variation in bacterial ribosomal drug-binding sites.","authors":"Chinenye L Ekemezie, Lewis I Chan, Charlotte R Brown, Karla Helena-Bueno, Tom A Williams, Sergey V Melnikov","doi":"10.1016/j.celrep.2025.115878","DOIUrl":"10.1016/j.celrep.2025.115878","url":null,"abstract":"<p><p>Ribosomes from certain bacteria possess divergent drug-binding sites compared to those of Escherichia coli, leading to natural evasion or hypersensitivity to antibiotics. However, in the absence of systematic studies, it is unknown whether this divergence is rare or common among bacterial species. Here, we address this by reconstructing the evolutionary history of drug-binding residues in bacterial ribosomes. We find that many rRNA residues that are currently viewed as bacterial-specific features of ribosomal drug-binding sites are in fact conserved only in a subset of bacteria. Conversely, species with divergent drug-binding sites are widespread in nature, arising from ancient rRNA polymorphisms at the direct ribosome-drug interface. Using a few bacterial species harboring divergent drug-binding sites, we identify their intrinsic resistance to corresponding ribosome-targeting antibiotics. Overall, we reveal the extensive lineage-specific diversity of ribosomal drug-binding sites, offering a resource for developing more targeted antibiotics and enabling personalized drug selection for specific pathogens.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115878"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-22Epub Date: 2025-06-19DOI: 10.1016/j.celrep.2025.115859
Petra Schneiderova, Jan Mizera, Arootin Gharibian, Gayane Manukyan, Milan Raska, Petr Gajdos, Petr Kosztyu, Samuel Genzor, Milos Kudelka, Milan Sova, Jakub Savara, Alena Borikova, Bishu Shrestha, Zuzana Mikulkova, Ladislav Stepanek, Jiri Kufa, Petr Jakubec, Eva Kriegova
{"title":"The SARS-CoV-2 trigger highlights host interleukin 1 genetics in Epstein-Barr virus reactivation.","authors":"Petra Schneiderova, Jan Mizera, Arootin Gharibian, Gayane Manukyan, Milan Raska, Petr Gajdos, Petr Kosztyu, Samuel Genzor, Milos Kudelka, Milan Sova, Jakub Savara, Alena Borikova, Bishu Shrestha, Zuzana Mikulkova, Ladislav Stepanek, Jiri Kufa, Petr Jakubec, Eva Kriegova","doi":"10.1016/j.celrep.2025.115859","DOIUrl":"10.1016/j.celrep.2025.115859","url":null,"abstract":"<p><p>Studies in large cohorts exposed to the same triggers associated with Epstein-Barr virus (EBV) reactivation and the follow-up of post-acute outcomes may uncover the pathomechanisms of autoimmune conditions and EBV-related cancer. We investigated a large cohort of individuals infected with SARS-CoV-2 infection reporting long COVID (LC) symptoms for positive serological markers of recent EBV reactivation (viral capsid antigen [VCA] immunoglobulin [Ig]M, VCA IgA, and early antigen D IgG), host interleukin (IL)1 and IL10 genetics, and immune response. Recent EBV reactivation occurs more frequently in individuals with a genetic risk of EBV reactivation in the IL1RN, IL1A, and IL1B genes associated with an elevated ratio of IL-1 receptor antagonist (IL-1Ra)/IL-1β and a higher latent EBV load in blood. High levels of anti-VCA IgA serve as a strong marker of recent EBV reactivation, which is associated with objective long-term pulmonary dysfunction in LC. Our data highlight the association between host IL1 genetics and EBV reactivation.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115859"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144336363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-22Epub Date: 2025-06-25DOI: 10.1016/j.celrep.2025.115904
Olivia Luyties, Lynn Sanford, Jessica Rodino, Michael Nagel, Taylor Jones, Jenna K Rimel, Christopher C Ebmeier, Megan Palacio, Grace S Shelby, Kira Cozzolino, Finn Brennan, Axel Hartzog, Mirzam B Saucedo, Lotte P Watts, Sabrina Spencer, Jennifer F Kugel, Robin D Dowell, Dylan J Taatjes
{"title":"Multi-omics and biochemical reconstitution reveal CDK7-dependent mechanisms controlling RNA polymerase II function at gene 5'- and 3' ends.","authors":"Olivia Luyties, Lynn Sanford, Jessica Rodino, Michael Nagel, Taylor Jones, Jenna K Rimel, Christopher C Ebmeier, Megan Palacio, Grace S Shelby, Kira Cozzolino, Finn Brennan, Axel Hartzog, Mirzam B Saucedo, Lotte P Watts, Sabrina Spencer, Jennifer F Kugel, Robin D Dowell, Dylan J Taatjes","doi":"10.1016/j.celrep.2025.115904","DOIUrl":"10.1016/j.celrep.2025.115904","url":null,"abstract":"<p><p>CDK7 regulates RNA polymerase II (RNAPII) initiation, elongation, and termination through incompletely understood mechanisms. Because contaminating kinases prevent reliable CDK7 analysis with nuclear extracts, we reconstitute RNAPII transcription with purified factors. We show that CDK7 inhibition slows and/or pauses RNAPII promoter-proximal transcription and suppresses re-initiation, and these effects are Mediator and TFIID dependent. Similarly in human cells, CDK7 inhibition reduces transcriptional output by suppressing RNAPII initiation and/or re-initiation. Moreover, widespread 3' end readthrough transcription occurs in CDK7-inhibited cells; mechanistically, this results from rapid nuclear depletion of RNAPII elongation and termination factors (e.g., DSIF, Integrator, NELF, SPT6, PPP1R10/PNUTS, and SCAF8), including high-confidence CDK7 kinase targets. Collectively, these results define how CDK7 governs RNAPII function at gene 5' ends and 3' ends and reveal that nuclear abundance of elongation and termination factors is kinase dependent. Because 3'-readthrough transcription is commonly induced during stress, our results further suggest that regulated suppression of CDK7 activity enables this transcriptional response.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115904"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144504879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-22Epub Date: 2025-06-24DOI: 10.1016/j.celrep.2025.115911
Qiuyuan Zhang, ZhuRong Deng, Xiaoxue Li, Jiao Qiao, Ziniu Li, Peipei Liu, Alfred M Handler, Bruno Lemaitre, Weiwei Zheng, Hongyu Zhang
{"title":"Gut commensal bacteria-derived methionine is required for host reproduction by modulating RNA m6A methylation of the insulin receptor.","authors":"Qiuyuan Zhang, ZhuRong Deng, Xiaoxue Li, Jiao Qiao, Ziniu Li, Peipei Liu, Alfred M Handler, Bruno Lemaitre, Weiwei Zheng, Hongyu Zhang","doi":"10.1016/j.celrep.2025.115911","DOIUrl":"10.1016/j.celrep.2025.115911","url":null,"abstract":"<p><p>Gut commensal bacteria promote host reproduction by modulating metabolism and nutrition, but the molecular mechanisms by which microbes regulate reproduction remain unclear. Here, we show that gut commensal bacteria promote host reproduction by providing the amino acid methionine, which controls the RNA m6A modification level of insulin receptor (InR) in the ovary of the invasive insect Bactrocera dorsalis. Antibiotic-treated B. dorsalis shows reduced RNA m6A methylation levels and methionine content, resulting in arrested ovarian development and decreased fecundity. The gut commensal bacterium Enterobacter hormaechei-derived metabolite methionine restores the decreased RNA m6A level and the reproductive defects. Notably, the knockdown of METTL3 and METTL14, two genes encoding the RNA m6A methyltransferases, reduces InR mRNA and protein levels and impairs ovarian development in B. dorsalis. Our findings further expand the functional landscape of RNA m6A modification to include nutrient-dependent control of ovarian development and highlight the essential role of epigenetic regulation in microbe-host interactions.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115911"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144494903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell reportsPub Date : 2025-07-22Epub Date: 2025-07-01DOI: 10.1016/j.celrep.2025.115933
Fauzia N Izzati, Hani Choksi, Paolo Giuliana, Diala Abd-Rabbo, Heidi Elsaesser, Aled Blundell, Vanessa Affe, Vinicius Kannen, Zeinab Jame-Chenarboo, Edward N Schmidt, Meggie Kuypers, David B Avila, Eric S Y Chiu, Dzhangar Badmaev, Haissi Cui, Jason Matthews, Thierry Mallevaey, Matthew S Macauley, David G Brooks, Landon J Edgar
{"title":"Presentation of immunoregulatory sialoglycans on T cells is divergent between mice and humans.","authors":"Fauzia N Izzati, Hani Choksi, Paolo Giuliana, Diala Abd-Rabbo, Heidi Elsaesser, Aled Blundell, Vanessa Affe, Vinicius Kannen, Zeinab Jame-Chenarboo, Edward N Schmidt, Meggie Kuypers, David B Avila, Eric S Y Chiu, Dzhangar Badmaev, Haissi Cui, Jason Matthews, Thierry Mallevaey, Matthew S Macauley, David G Brooks, Landon J Edgar","doi":"10.1016/j.celrep.2025.115933","DOIUrl":"10.1016/j.celrep.2025.115933","url":null,"abstract":"<p><p>Glycans are emerging as important regulators of T cell function but remain poorly characterized across the functionally distinct populations that exist in vivo. Here, we couple single-cell analysis technologies with soluble lectins and chemical probes to interrogate glycosylation patterns on major T cell populations across mouse and human tissues. Our analysis focused on terminal glycan epitopes with immunomodulatory functions, including sialoglycan ligands for Siglecs. We demonstrate that glycosylation patterns are diverse across the resting murine T cell repertoire and dynamically remodeled in response to stimulation. Surprisingly, we find that human T cell populations do not share the same glycoprofiles or glycan remodeling dynamics as their murine counterparts. We show that these differences can be explained by divergent regulation of glycan biosynthesis pathways between the species. These results highlight fundamental glycophysiological differences between mouse and human T cells and reveal features that are critical to consider for glycan-targeted therapies.</p>","PeriodicalId":9798,"journal":{"name":"Cell reports","volume":"44 7","pages":"115933"},"PeriodicalIF":6.9,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144559333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}