Developmental cell最新文献_第10页

Chromatin-associated PP1 subcomplexes: Together, but not in each other's pockets. 染色质相关的PP1亚复合物：在一起，但不在彼此的口袋里。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 DOI: 10.1016/j.devcel.2026.04.002

Sergio Moreno, Sandra Lopez-Aviles

引用次数: 0

CD155-CD96 keeps quiescent persister tumor cells in check. CD155-CD96控制静止的持久性肿瘤细胞。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 DOI: 10.1016/j.devcel.2026.04.007

Johanna M Gorol, Florian R Greten

引用次数: 0

Multi-omic analyses reveal a differential contribution of chromatin-associated PP1 holoenzymes to mitotic exit and G1 re-establishment. 多组学分析揭示了染色质相关的PP1全酶对有丝分裂退出和G1重建的差异贡献。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 Epub Date: 2026-03-17 DOI: 10.1016/j.devcel.2026.02.016

Konstantinos Stamatiou, Florentin Huguet, Marta Budzinska, Jose I de Las Heras, Denise Ragusa, Ines J deCastro, Christos Spanos, Juri Rappsilberg, Paola Vagnarelli

{"title":"Multi-omic analyses reveal a differential contribution of chromatin-associated PP1 holoenzymes to mitotic exit and G1 re-establishment.","authors":"Konstantinos Stamatiou, Florentin Huguet, Marta Budzinska, Jose I de Las Heras, Denise Ragusa, Ines J deCastro, Christos Spanos, Juri Rappsilberg, Paola Vagnarelli","doi":"10.1016/j.devcel.2026.02.016","DOIUrl":"10.1016/j.devcel.2026.02.016","url":null,"abstract":"Mitotic exit is an important part of the cell cycle, requiring the coordination of many chromatin and cytoskeleton remodeling events to successfully complete cell division and maintain cell identity. Protein dephosphorylation is a key step in directing mitotic exit, and protein phosphatase 1 (PP1) is essential to this process; however, the specific contribution of its numerous targeting subunits is still unknown. Here, we have investigated the function of three chromatin-associated PP1-targeting subunits in mitosis exit: Repo-Man, Ki-67, and protein phosphatase 1 nuclear targeting subunit (PNUTS). We generated endogenously tagged, auxin-degradable alleles for each subunit in the human cell line HCT116 and used a multi-omic approach to address their specific contributions toward transcription resumption, chromatin accessibility, and protein dephosphorylation at the transition from mitosis to G1. This approach identified their distinct role in mitotic exit, provided datasets for the cell-cycle community, and highlighted functions for Ki-67 and Repo-Man in genome stability and organization.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"1127-1145.e8"},"PeriodicalIF":9.2,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147480052","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}

引用次数: 0

Additional layers of systemic plant immunity: Apoplastic pH and uORF peptides. 系统植物免疫的附加层：胞外pH和uORF肽。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 DOI: 10.1016/j.devcel.2026.04.008

Hannah Weber, Birgit Kemmerling

引用次数: 0

The want for Wnt: Pancreatic cancer assembles a self-sustaining Wnt-signaling ecosystem. 对Wnt的需求：胰腺癌组装了一个自我维持的Wnt信号生态系统。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 DOI: 10.1016/j.devcel.2026.04.010

Nikki K Lytle, Laura D Wood

引用次数: 0

Single-molecule mitochondrial DNA imaging reveals heteroplasmy dynamics shaped by developmental bottlenecks and selection in vivo. 单分子线粒体DNA成像揭示了体内发育瓶颈和选择形成的异质性动力学。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-05-13 DOI: 10.1016/j.devcel.2026.03.011

Rajini Chandrasegaram, Sara Gottardo, Abhilesh Dhawanjewar, Antony M Hynes-Allen, Beitong Gao, Suvagata Roy Chowdhury, Luis-Carlos Tábara, Michele Frison, Stavroula Petridi, Patrick F Chinnery, Julien Prudent, Hansong Ma, Jelle van den Ameele

{"title":"Single-molecule mitochondrial DNA imaging reveals heteroplasmy dynamics shaped by developmental bottlenecks and selection in vivo.","authors":"Rajini Chandrasegaram, Sara Gottardo, Abhilesh Dhawanjewar, Antony M Hynes-Allen, Beitong Gao, Suvagata Roy Chowdhury, Luis-Carlos Tábara, Michele Frison, Stavroula Petridi, Patrick F Chinnery, Julien Prudent, Hansong Ma, Jelle van den Ameele","doi":"10.1016/j.devcel.2026.03.011","DOIUrl":"10.1016/j.devcel.2026.03.011","url":null,"abstract":"Mitochondrial DNA (mtDNA) exists in many copies per cell, with cell-to-cell variability in mutation load, which is known as heteroplasmy. Developmental and age-related expansion of heteroplasmic mtDNA mutations contributes to the pathogenesis of mitochondrial and neurodegenerative diseases. Here, we describe an approach for in situ sequence-specific detection of single mtDNA molecules (mtDNA-single-molecule fluorescent in situ hybridization [smFISH]). We apply this method to visualize and measure mtDNA and heteroplasmy levels in situ at single-cell resolution in whole-mount Drosophila tissue and cultured human cells. In Drosophila, we identify a somatic mtDNA bottleneck during neurogenesis. This amplifies heteroplasmy variability between neurons, as predicted by a mathematical bottleneck model, predisposing individual neurons to a high mutation load. However, both during neurogenesis and oogenesis, mtDNA segregation is accompanied by purifying selection, promoting wild-type (WT) over pathogenic mtDNA. mtDNA-smFISH thus elucidates how developmental cell-fate transitions, accompanied by changes in cell morphology, behavior, and metabolism, can shape the transmission and selection of deleterious mtDNA variants.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"61 5","pages":"1146-1161.e8"},"PeriodicalIF":9.2,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7619573/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147927399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

A skeletal muscle atlas shows neuromuscular junction adaptations to growth and atrophy 骨骼肌图谱显示神经肌肉连接适应生长和萎缩

IF 11.8 1区生物学

Developmental cell Pub Date : 2026-04-21 DOI: 10.1016/j.devcel.2026.03.010

Silvia Campanario, Mercedes Grima-Terrén, Megan Rommelfanger, Stefania Dell’ Orso, Xuesong Feng, Andrés Cisneros, Ignacio Ramírez-Pardo, Aina Calls-Cobos, Benjamin A. Yang, Kyung Dae Ko, Esther García-Domínguez, Laura Pena-Couso, Grace Chou, Yuewen Zheng, Nasun Hah, Davide Randazzo, Alberto Pérez-Garcia, Tovah E. Markowitz, Jose Milisenda, Iago Pinal-Fernandez, Pura Muñoz-Cánoves

{"title":"A skeletal muscle atlas shows neuromuscular junction adaptations to growth and atrophy","authors":"Silvia Campanario, Mercedes Grima-Terrén, Megan Rommelfanger, Stefania Dell’ Orso, Xuesong Feng, Andrés Cisneros, Ignacio Ramírez-Pardo, Aina Calls-Cobos, Benjamin A. Yang, Kyung Dae Ko, Esther García-Domínguez, Laura Pena-Couso, Grace Chou, Yuewen Zheng, Nasun Hah, Davide Randazzo, Alberto Pérez-Garcia, Tovah E. Markowitz, Jose Milisenda, Iago Pinal-Fernandez, Pura Muñoz-Cánoves","doi":"10.1016/j.devcel.2026.03.010","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.010","url":null,"abstract":"The molecular basis underlying muscle atrophy, as it occurs during disuse or aging, and activity-induced hypertrophy remain poorly understood. A major challenge has been defining the diverse cellular and niche environments within skeletal muscle, which is mostly composed of multinucleated myofibers. Here, we present a single-nucleus and single-cell transcriptomic atlas, coupled with spatial profiling, of mouse limb skeletal muscle under resting conditions and during experimentally induced atrophy or hypertrophy. We identify condition-dependent shifts in muscle-resident cell populations and fiber-type-specific transcriptional responses. We also uncover extensive remodeling of the neuromuscular junction (NMJ), including the emergence of specialized synaptic myonuclei (SynM) and terminal Schwann cells (tSCs) associated with atrophic or hypertrophic states. High-resolution 3D imaging and spatial transcriptomics confirm these changes at the tissue level. Similar NMJ alterations are observed in denervated and exercised human muscle, supporting the translational relevance of this atlas for studying muscle plasticity and identifying therapeutic targets in muscle-related diseases.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"136 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147726414","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}

引用次数: 0

AMBRA1 enhances Sonic Hedgehog signaling during cerebellar development and in medulloblastoma AMBRA1在小脑发育和成神经管细胞瘤中增强Sonic Hedgehog信号

IF 11.8 1区生物学

Developmental cell Pub Date : 2026-04-13 DOI: 10.1016/j.devcel.2026.03.008

Irene Basili, Francesca Bufalieri, Marilisa Conenna, Shirin Navacci, Yue-Ru Li, Jacob Torrejon, Flavia Bernardi, Ludovica Lospinoso Severini, Veronique Marsaud, Gabriele Cancila, Guillaume Bourmeau, Hua Yu, Valentina Lo Re, Julie Talbot, Gennaro Adabbo, Alberico Di Pinto, Francesca Agnoli, Daniela Giovannini, Simona Leonardi, Rosa Bordone, Lucia Di Marcotullio

{"title":"AMBRA1 enhances Sonic Hedgehog signaling during cerebellar development and in medulloblastoma","authors":"Irene Basili, Francesca Bufalieri, Marilisa Conenna, Shirin Navacci, Yue-Ru Li, Jacob Torrejon, Flavia Bernardi, Ludovica Lospinoso Severini, Veronique Marsaud, Gabriele Cancila, Guillaume Bourmeau, Hua Yu, Valentina Lo Re, Julie Talbot, Gennaro Adabbo, Alberico Di Pinto, Francesca Agnoli, Daniela Giovannini, Simona Leonardi, Rosa Bordone, Lucia Di Marcotullio","doi":"10.1016/j.devcel.2026.03.008","DOIUrl":"https://doi.org/10.1016/j.devcel.2026.03.008","url":null,"abstract":"AMBRA1 (autophagy and beclin 1 regulator 1) is primarily recognized as a tumor suppressor. However, its role as a tumor promoter has garnered increasing attention. Here, leveraging clinical data of an international multi-omic medulloblastoma (MB) cohort, we identified that elevated AMBRA1 protein levels, independently of its mRNA expression, correlate with poor prognosis in the Sonic Hedgehog subgroup (MBSHH). Mechanistically, AMBRA1 enhances SHH signaling by stabilizing GLI1, the pathway’s final effector, via inhibition of its βTrCP-mediated degradation. Additionally, AMBRA1 protein stability is modulated by the REN E3 ubiquitin ligase, a tumor suppressor gene lost in MBSHH. Inhibition of AMBRA1 blocks MBSHH growth in murine and patient-derived preclinical models. Moreover, combining AMBRA1 knockdown with FDA-approved SHH inhibitors enhances antitumor efficacy. These findings identify the AMBRA1/βTrCP/REN axis as a key regulatory mechanism in SHH signaling and discover an unrecognized function of AMBRA1 in MBSHH, providing actionable insights into brain tumor biology.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":"5 1","pages":""},"PeriodicalIF":11.8,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147666430","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}

引用次数: 0

Insolubilome profiling defines molecular features that influence protein insolubility with aging. 不溶性组谱定义了影响蛋白质不溶性随年龄增长的分子特征。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-04-08 Epub Date: 2026-02-19 DOI: 10.1016/j.devcel.2026.01.015

Anna Stephan, Flavia A Graca, Vishwajeeth R Pagala, Liam C Hunt, Chia-Lung Chuang, John Grime, Daniel Alford, Xusheng Wang, Anthony A High, Junmin Peng, Fabio Demontis

{"title":"Insolubilome profiling defines molecular features that influence protein insolubility with aging.","authors":"Anna Stephan, Flavia A Graca, Vishwajeeth R Pagala, Liam C Hunt, Chia-Lung Chuang, John Grime, Daniel Alford, Xusheng Wang, Anthony A High, Junmin Peng, Fabio Demontis","doi":"10.1016/j.devcel.2026.01.015","DOIUrl":"10.1016/j.devcel.2026.01.015","url":null,"abstract":"Solubility regulates protein function, but how it is governed by aging remains elusive. Here, we utilized mass spectrometry to define the relative composition of the soluble and insoluble tissue/organ fractions during mouse aging. In the young, there is a wide (∼100-1,000×) range of insoluble/soluble protein ratios that differ tissue-specifically. With aging, some proteins become relatively more insoluble, while others are conversely regulated or unaffected. Age-related insoluble/soluble changes are not merely dictated by histological similarity, diverge in related tissues with distinct degeneration propensities, and correlate tissue-specifically with structural features. Proteins that become age-insoluble in multiple organs include aggregation-prone circulating factors and ectopically expressed proteins. For instance, although primarily expressed by the epidermis, hornerin insolubility increases with aging in skeletal muscle, and experimental hornerin upregulation causes muscle weakness. Thus, age-insoluble proteins are useful biomarkers but can also contribute to age-related functional decline, highlighting a multifaceted remodeling of the insolubilome with aging.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"936-958.e7"},"PeriodicalIF":9.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257717","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}

引用次数: 0

Bmp9 regulates Notch signaling and the temporal dynamics of angiogenesis via Lunatic Fringe. Bmp9通过Lunatic Fringe调控Notch信号和血管生成的时间动态。

IF 9.2 1区生物学

Developmental cell Pub Date : 2026-04-08 Epub Date: 2026-02-05 DOI: 10.1016/j.devcel.2026.01.006

Tommaso Ristori, Raphael Thuret, Erika Hooker, Peter Quicke, Sami Sanlidag, Kevin Lanthier, Kalonji Ntumba, Irene M Aspalter, Marina Uroz, Cecilia M Sahlgren, Shane P Herbert, Christopher S Chen, Bruno Larrivée, Katie Bentley

{"title":"Bmp9 regulates Notch signaling and the temporal dynamics of angiogenesis via Lunatic Fringe.","authors":"Tommaso Ristori, Raphael Thuret, Erika Hooker, Peter Quicke, Sami Sanlidag, Kevin Lanthier, Kalonji Ntumba, Irene M Aspalter, Marina Uroz, Cecilia M Sahlgren, Shane P Herbert, Christopher S Chen, Bruno Larrivée, Katie Bentley","doi":"10.1016/j.devcel.2026.01.006","DOIUrl":"10.1016/j.devcel.2026.01.006","url":null,"abstract":"Sprouting angiogenesis and blood vessel stabilization require precise coordination between endothelial cells (ECs) and pericytes. Bone Morphogenic Protein 9 (Bmp9), whose signaling through activin receptor-like kinase 1 (Alk1) is dysregulated in several diseases, was thought to regulate these processes by independently activating Notch target genes in an additive fashion with canonical Notch signaling. Here, through predictive computational modeling validated in mice, zebrafish, and human cell lines, we uncover that Bmp9 enhances Notch activity synergistically by upregulating Lunatic Fringe (Lfng) in ECs. Specifically, Bmp9-induced Lfng enhances Notch receptor activation, most strongly when Delta-like ligand 4 (Dll4) is also present. This Lfng regulation alters vessel branching by modulating the timing of EC phenotype selection and rearrangement during angiogenesis. Lfng also contributes to pericyte-driven vessel stabilization by mediating Jagged1 upregulation in Bmp9-stimulated ECs. In summary, Bmp9-upregulated Lfng enhances Dll4-Notch1 signaling in ECs and Jag1-Notch3 activation in pericytes, shaping angiogenic sprouting and stabilization outcomes.","PeriodicalId":11157,"journal":{"name":"Developmental cell","volume":" ","pages":"837-853.e9"},"PeriodicalIF":9.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13407922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146131489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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