Pub Date : 2025-10-02DOI: 10.1038/s41580-025-00906-4
Christina Marie Termini
Christina Termini highlights the importance of the identification of haematopoietic stem cell markers.
Christina Termini强调了鉴定造血干细胞标记物的重要性。
{"title":"SLAM passes the haematopoietic stem cell identity test","authors":"Christina Marie Termini","doi":"10.1038/s41580-025-00906-4","DOIUrl":"10.1038/s41580-025-00906-4","url":null,"abstract":"Christina Termini highlights the importance of the identification of haematopoietic stem cell markers.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"27 1","pages":"9-9"},"PeriodicalIF":90.2,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145209286","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}
Pub Date : 2025-10-01DOI: 10.1038/s41580-025-00910-8
Kim Baumann
Colon stem cells expressing the surface markers NOX1 and NPY1R can give rise to colon cancer in mice.
表达表面标记物NOX1和NPY1R的结肠干细胞可引起小鼠结肠癌。
{"title":"Stem cell sources of colon cancer in mice","authors":"Kim Baumann","doi":"10.1038/s41580-025-00910-8","DOIUrl":"10.1038/s41580-025-00910-8","url":null,"abstract":"Colon stem cells expressing the surface markers NOX1 and NPY1R can give rise to colon cancer in mice.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"26 11","pages":"823-823"},"PeriodicalIF":90.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145203556","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}
Pub Date : 2025-10-01DOI: 10.1038/s41580-025-00905-5
Sean Munro
The advent of laser-scanning confocal microscopy revolutionized cell biology, offering unprecedented resolution and depth and enabling scientists to visualize cellular structures in 3D.
Pub Date : 2025-09-30DOI: 10.1038/s41580-025-00882-9
Tony Tiganis, Nicholas K. Tonks
Aberrations in protein tyrosine phosphorylation-dependent cell signalling contribute to a wide variety of human diseases. Drugs targeting protein tyrosine kinases have had a major impact on human health; by contrast, protein tyrosine phosphatases (PTPs), which serve unique functions and together with protein tyrosine kinases coordinate tyrosine phosphorylation-dependent cell signalling, have been underexploited therapeutically. In this Review, we discuss key breakthroughs in our understanding of how PTPs are regulated, highlight their capacity to coordinate signalling and provide examples of their complex roles in physiology and pathophysiology, including diabetes, obesity and cancer. Also, we discuss the development of PTP-targeted therapeutics that are in clinical trials or poised for clinical translation. We argue that the emergence of this class of enzymes from the shadows lays the foundation for a more complete understanding of the regulation of cell signalling and heralds a new era of drug development opportunities to combat important human diseases. Protein tyrosine phosphatases (PTPs) regulate cell signalling and contribute to a wide range of human diseases. This Review discusses mechanistic insights into PTP function and regulation, their physiological roles and the development of PTP-targeted therapeutics.
{"title":"Mechanisms, functions and therapeutic targeting of protein tyrosine phosphatases","authors":"Tony Tiganis, Nicholas K. Tonks","doi":"10.1038/s41580-025-00882-9","DOIUrl":"10.1038/s41580-025-00882-9","url":null,"abstract":"Aberrations in protein tyrosine phosphorylation-dependent cell signalling contribute to a wide variety of human diseases. Drugs targeting protein tyrosine kinases have had a major impact on human health; by contrast, protein tyrosine phosphatases (PTPs), which serve unique functions and together with protein tyrosine kinases coordinate tyrosine phosphorylation-dependent cell signalling, have been underexploited therapeutically. In this Review, we discuss key breakthroughs in our understanding of how PTPs are regulated, highlight their capacity to coordinate signalling and provide examples of their complex roles in physiology and pathophysiology, including diabetes, obesity and cancer. Also, we discuss the development of PTP-targeted therapeutics that are in clinical trials or poised for clinical translation. We argue that the emergence of this class of enzymes from the shadows lays the foundation for a more complete understanding of the regulation of cell signalling and heralds a new era of drug development opportunities to combat important human diseases. Protein tyrosine phosphatases (PTPs) regulate cell signalling and contribute to a wide range of human diseases. This Review discusses mechanistic insights into PTP function and regulation, their physiological roles and the development of PTP-targeted therapeutics.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"27 2","pages":"129-152"},"PeriodicalIF":90.2,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145194782","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}
Pub Date : 2025-09-29DOI: 10.1038/s41580-025-00899-0
Hesso Farhan, Ishier Raote, Felix Campelo, Liang Ge, Koret Hirschberg, Alison Forrester, Giulia Zanetti, Jennifer Lippincott-Schwartz, José Carlos Pastor-Pareja, Franck Perez, Kota Saito, Vivek Malhotra
Endoplasmic reticulum exit sites (ERES) are specialized, ribosome-free ER subdomains that serve as dynamic portals for COPII-mediated export of proteins from the ER. Beyond their role in the secretory pathway, ERES are implicated in diverse processes, including autophagy and the maturation of lipid droplets, highlighting their functional plasticity. ERES integrate cargo load, membrane tension and spatial cues to remodel their architecture and function in real time. This Roadmap synthesizes our current knowledge on the biogenesis, structural diversity and regulatory logic of ERES. We highlight key unanswered questions in the field, particularly concerning how ERES integrate signals to coordinate protein trafficking under varying cellular states. Finally, we propose a multidisciplinary framework — leveraging advances in high-resolution imaging, synthetic reconstitution and computational modelling — to delineate the principles governing the function and plasticity of ERES. Understanding these mechanisms holds significant potential for developing targeted therapeutic strategies in diseases linked to trafficking dysfunction. Endoplasmic reticulum exit sites (ERES) are specialized ER subdomains that regulate the export of secreted cargo. This Roadmap explores how ERES integrate biochemical and mechanical signals to coordinate trafficking and proposes a multidisciplinary strategy to investigate their function, including in disease.
{"title":"Towards a unified framework for the function of endoplasmic reticulum exit sites","authors":"Hesso Farhan, Ishier Raote, Felix Campelo, Liang Ge, Koret Hirschberg, Alison Forrester, Giulia Zanetti, Jennifer Lippincott-Schwartz, José Carlos Pastor-Pareja, Franck Perez, Kota Saito, Vivek Malhotra","doi":"10.1038/s41580-025-00899-0","DOIUrl":"10.1038/s41580-025-00899-0","url":null,"abstract":"Endoplasmic reticulum exit sites (ERES) are specialized, ribosome-free ER subdomains that serve as dynamic portals for COPII-mediated export of proteins from the ER. Beyond their role in the secretory pathway, ERES are implicated in diverse processes, including autophagy and the maturation of lipid droplets, highlighting their functional plasticity. ERES integrate cargo load, membrane tension and spatial cues to remodel their architecture and function in real time. This Roadmap synthesizes our current knowledge on the biogenesis, structural diversity and regulatory logic of ERES. We highlight key unanswered questions in the field, particularly concerning how ERES integrate signals to coordinate protein trafficking under varying cellular states. Finally, we propose a multidisciplinary framework — leveraging advances in high-resolution imaging, synthetic reconstitution and computational modelling — to delineate the principles governing the function and plasticity of ERES. Understanding these mechanisms holds significant potential for developing targeted therapeutic strategies in diseases linked to trafficking dysfunction. Endoplasmic reticulum exit sites (ERES) are specialized ER subdomains that regulate the export of secreted cargo. This Roadmap explores how ERES integrate biochemical and mechanical signals to coordinate trafficking and proposes a multidisciplinary strategy to investigate their function, including in disease.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"26 12","pages":"957-969"},"PeriodicalIF":90.2,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145189269","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}
Pub Date : 2025-09-26DOI: 10.1038/s41580-025-00903-7
Jonathan N. Pruneda, Roko Žaja, Michael S. Cohen, Karla L. H. Feijs-Žaja
Evidence is mounting that crosstalk between ubiquitylation and ADP-ribosylation is crucial for maintaining proteostasis. Recent studies have revealed that mono(ADP-ribose) can recruit and activate specific ubiquitin E3 ligases. In this Comment, we discuss MARUbylation — the (literal) linking of mono(ADP-ribose) and ubiquitin into a distinct new hybrid modification. A newly discovered hybrid protein modification of mono(ADP-ribose) and ubiquitin is recognized by dedicated effectors that promote processing of the modified proteins.
{"title":"The emergence of MARUbe — a hybrid ADP-ribose–ubiquitin modification","authors":"Jonathan N. Pruneda, Roko Žaja, Michael S. Cohen, Karla L. H. Feijs-Žaja","doi":"10.1038/s41580-025-00903-7","DOIUrl":"10.1038/s41580-025-00903-7","url":null,"abstract":"Evidence is mounting that crosstalk between ubiquitylation and ADP-ribosylation is crucial for maintaining proteostasis. Recent studies have revealed that mono(ADP-ribose) can recruit and activate specific ubiquitin E3 ligases. In this Comment, we discuss MARUbylation — the (literal) linking of mono(ADP-ribose) and ubiquitin into a distinct new hybrid modification. A newly discovered hybrid protein modification of mono(ADP-ribose) and ubiquitin is recognized by dedicated effectors that promote processing of the modified proteins.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"26 11","pages":"820-821"},"PeriodicalIF":90.2,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145153416","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}
Pub Date : 2025-09-24DOI: 10.1038/s41580-025-00878-5
Sasha Mendjan, Alison Deyett, Deborah Yelon
Heart development has been extensively explored on the anatomical, cellular and molecular levels. Yet, the intricate interplay of tissue organization, cellular lineages and molecular factors that orchestrate heart development, culminating in forming a seamlessly synchronized functional heart, remains challenging to investigate. Mechanistic studies conducted both in vivo using animal models and in vitro stem-cell-derived systems aim to unravel this complexity. In this Review, we discuss how the recent surge in technological advancements in imaging and genomics, coupled with the evolution of next-generation cardiac organoid models, has provided profound insights into these processes, holding significant implications for the development of novel therapies for congenital or acquired heart diseases. We discuss the development of the heart as the first functional organ — from the morphogenesis of the mesoderm, heart tube and cardiac chambers to the establishment of the initial heartbeat and pacemaker and further how morphogenesis and function collaboratively drive heart maturation. The development of a functional heart depends on the specification of multiple cell types, including pacemaker cells, and complex tissue re-organization. This Review discusses recent insights into these processes from in vivo studies and cardiac organoid models.
{"title":"Coordination of cardiogenesis in vivo and in vitro","authors":"Sasha Mendjan, Alison Deyett, Deborah Yelon","doi":"10.1038/s41580-025-00878-5","DOIUrl":"10.1038/s41580-025-00878-5","url":null,"abstract":"Heart development has been extensively explored on the anatomical, cellular and molecular levels. Yet, the intricate interplay of tissue organization, cellular lineages and molecular factors that orchestrate heart development, culminating in forming a seamlessly synchronized functional heart, remains challenging to investigate. Mechanistic studies conducted both in vivo using animal models and in vitro stem-cell-derived systems aim to unravel this complexity. In this Review, we discuss how the recent surge in technological advancements in imaging and genomics, coupled with the evolution of next-generation cardiac organoid models, has provided profound insights into these processes, holding significant implications for the development of novel therapies for congenital or acquired heart diseases. We discuss the development of the heart as the first functional organ — from the morphogenesis of the mesoderm, heart tube and cardiac chambers to the establishment of the initial heartbeat and pacemaker and further how morphogenesis and function collaboratively drive heart maturation. The development of a functional heart depends on the specification of multiple cell types, including pacemaker cells, and complex tissue re-organization. This Review discusses recent insights into these processes from in vivo studies and cardiac organoid models.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"27 1","pages":"19-34"},"PeriodicalIF":90.2,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145133933","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}
Pub Date : 2025-09-22DOI: 10.1038/s41580-025-00892-7
Monther Abu-Remaileh, Chii Jou Chan, Leilei Chen, Gozde S. Demirer, Ana Fiszbein, Florian Jug, Ana Victoria Lechuga-Vieco, Raphaëlle Luisier, Julia Pagan, Benjamin R. Sabari, Sichen Shao, Liming Sun, Jan J. Żylicz
To celebrate the journal’s 25th anniversary, we asked 13 researchers to offer a glimpse of what their research field might look like in 2050. They consider how technological breakthroughs — for example, artificial intelligence-powered virtual cells — could transform our understanding of how molecules, organelles and cells behave in different contexts, revolutionize therapies and enable the design of resilient crops.
{"title":"Visions of the future of molecular cell biology","authors":"Monther Abu-Remaileh, Chii Jou Chan, Leilei Chen, Gozde S. Demirer, Ana Fiszbein, Florian Jug, Ana Victoria Lechuga-Vieco, Raphaëlle Luisier, Julia Pagan, Benjamin R. Sabari, Sichen Shao, Liming Sun, Jan J. Żylicz","doi":"10.1038/s41580-025-00892-7","DOIUrl":"10.1038/s41580-025-00892-7","url":null,"abstract":"To celebrate the journal’s 25th anniversary, we asked 13 researchers to offer a glimpse of what their research field might look like in 2050. They consider how technological breakthroughs — for example, artificial intelligence-powered virtual cells — could transform our understanding of how molecules, organelles and cells behave in different contexts, revolutionize therapies and enable the design of resilient crops.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"26 10","pages":"735-740"},"PeriodicalIF":90.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111432","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}
Pub Date : 2025-09-22DOI: 10.1038/s41580-025-00904-6
Kim Baumann
Acute kidney injury induces somatic mitochondrial DNA mutations that impair energy metabolism and the resilience of kidney tissue to following injuries.
急性肾损伤诱导体细胞线粒体DNA突变，损害肾组织的能量代谢和对后续损伤的恢复能力。
{"title":"Tissue injury leads to the accumulation of somatic mtDNA mutations","authors":"Kim Baumann","doi":"10.1038/s41580-025-00904-6","DOIUrl":"10.1038/s41580-025-00904-6","url":null,"abstract":"Acute kidney injury induces somatic mitochondrial DNA mutations that impair energy metabolism and the resilience of kidney tissue to following injuries.","PeriodicalId":19051,"journal":{"name":"Nature Reviews Molecular Cell Biology","volume":"26 11","pages":"822-822"},"PeriodicalIF":90.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117044","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}
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