Pub Date : 2025-10-01Epub Date: 2025-07-28DOI: 10.1016/j.semcdb.2025.103637
Romain Levayer
{"title":"Special issue: “Novel functions of programmed cell death in development: Current status and future challenges”","authors":"Romain Levayer","doi":"10.1016/j.semcdb.2025.103637","DOIUrl":"10.1016/j.semcdb.2025.103637","url":null,"abstract":"","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"174 ","pages":"Article 103637"},"PeriodicalIF":6.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-02DOI: 10.1016/j.semcdb.2025.103623
Dorothee Bornhorst , Newsha Mortazavi , Felix Gunawan
Endothelial cells (ECs), which line the inner surface of blood vessels, continuously respond to biomechanical forces from blood flow, extracellular matrix, and intracellular tension. Recent advances have highlighted the pivotal role of these forces in regulating cellular plasticity during endothelial-to-hematopoietic transition (EHT) and endothelial-to-mesenchymal transition (EndMT), two processes essential for embryogenesis, tissue repair, and disease progression. EHT contributes to hematopoietic stem cell formation, and EndMT to valve formation and vessel sprouting. When misregulated, both processes cause vascular pathologies such as fibrosis, cancer metastasis, and atherosclerosis. This review provides an overview of how biomechanical cues influence EC fate decisions and behavioral transitions. We explore how external biomechanical forces are sensed at the endothelial cell surface, transmitted through intracellular adaptors, and affect changes at the transcriptional level. Understanding these mechanotransduction pathways during cell fate transition not only deepens our knowledge of endothelial cell plasticity but also provides insight into potential root causes of and treatments for vascular diseases.
{"title":"Force of change: How biomechanical cues drive endothelial plasticity and morphogenesis","authors":"Dorothee Bornhorst , Newsha Mortazavi , Felix Gunawan","doi":"10.1016/j.semcdb.2025.103623","DOIUrl":"10.1016/j.semcdb.2025.103623","url":null,"abstract":"<div><div>Endothelial cells (ECs), which line the inner surface of blood vessels, continuously respond to biomechanical forces from blood flow, extracellular matrix, and intracellular tension. Recent advances have highlighted the pivotal role of these forces in regulating cellular plasticity during endothelial-to-hematopoietic transition (EHT) and endothelial-to-mesenchymal transition (EndMT), two processes essential for embryogenesis, tissue repair, and disease progression. EHT contributes to hematopoietic stem cell formation, and EndMT to valve formation and vessel sprouting. When misregulated, both processes cause vascular pathologies such as fibrosis, cancer metastasis, and atherosclerosis. This review provides an overview of how biomechanical cues influence EC fate decisions and behavioral transitions. We explore how external biomechanical forces are sensed at the endothelial cell surface, transmitted through intracellular adaptors, and affect changes at the transcriptional level. Understanding these mechanotransduction pathways during cell fate transition not only deepens our knowledge of endothelial cell plasticity but also provides insight into potential root causes of and treatments for vascular diseases.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"173 ","pages":"Article 103623"},"PeriodicalIF":6.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144561060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-15DOI: 10.1016/j.semcdb.2025.103627
Brendan Capey, Shane P. Herbert
During tissue development, growth and regeneration, assembly of almost all new blood and lymphatic vessels arises via their branching from pre-existing vessels, processes termed angiogenesis and lymphangiogenesis, respectively. Furthermore, imbalances in these branching processes contribute to numerous disease states, including cancer, blindness, arthritis and ischemic disorders. At its core, new vessel branching is driven by the coordinated collective migration of specialized endothelial “tip” cells that lead sprouting vessels and “stalk” cells that trail the tip. Thus, studies defining the fundamental mechanisms directing angiogenesis and lymphangiogenesis not only have key therapeutic implications but have also defined core conserved principles dictating collective cell migration. In this review we focus on recent insights into the roles of intracellular, intercellular and cell morphology-driven positive- and negative-feedback loops in the establishment and maintenance of tip versus stalk cell identities and behaviour. Moreover, we highlight recent insights into the role of asymmetric cell divisions in self-organisation of the tip-stalk cell hierarchy during vessel assembly. Considering that many of the principles underpinning collective movement are broadly conserved between tissue systems, concepts described here likely play key roles in the control of collective cell migration in diverse tissue contexts.
{"title":"Establishment & maintenance of collective cell migration in angiogenesis: Lessons from zebrafish","authors":"Brendan Capey, Shane P. Herbert","doi":"10.1016/j.semcdb.2025.103627","DOIUrl":"10.1016/j.semcdb.2025.103627","url":null,"abstract":"<div><div>During tissue development, growth and regeneration, assembly of almost all new blood and lymphatic vessels arises via their branching from pre-existing vessels, processes termed angiogenesis and lymphangiogenesis, respectively. Furthermore, imbalances in these branching processes contribute to numerous disease states, including cancer, blindness, arthritis and ischemic disorders. At its core, new vessel branching is driven by the coordinated collective migration of specialized endothelial “tip” cells that lead sprouting vessels and “stalk” cells that trail the tip. Thus, studies defining the fundamental mechanisms directing angiogenesis and lymphangiogenesis not only have key therapeutic implications but have also defined core conserved principles dictating collective cell migration. In this review we focus on recent insights into the roles of intracellular, intercellular and cell morphology-driven positive- and negative-feedback loops in the establishment and maintenance of tip versus stalk cell identities and behaviour. Moreover, we highlight recent insights into the role of asymmetric cell divisions in self-organisation of the tip-stalk cell hierarchy during vessel assembly. Considering that many of the principles underpinning collective movement are broadly conserved between tissue systems, concepts described here likely play key roles in the control of collective cell migration in diverse tissue contexts.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"173 ","pages":"Article 103627"},"PeriodicalIF":6.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144631760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-08DOI: 10.1016/j.semcdb.2025.103629
Tony Yu-Chen Tsai , Diana Pinheiro
An outstanding question in biology is how tissue patterning emerges during development. The concept of positional information, which posits that gradients of morphogens instruct cell fate in a concentration-dependent manner, has been an influential framework to understand pattern formation. Recent studies, however, highlight that developing tissues are highly dynamic, with cellular movements, arising from local mechanical fluctuations or global morphogenetic forces, that often coincide with morphogen signaling and cell fate specification. This calls for a more dynamic understanding of pattern formation by explicitly investigating the interplay between signaling, cell fate and morphogenesis. In this review, we first discuss emerging evidence on the role of cellular movements in modulating signaling dosage and cell fate acquisition. We then examine the biophysical strategies employed by developing tissues to achieve robust patterning despite ongoing cellular dynamics and large-scale morphogenesis. While cellular movements may intuitively be viewed as disruptive to patterning programs, recent evidence suggests that when coupled with cell fate, they can act as a critical mechanism for generating and stabilizing precise tissue patterns during development.
{"title":"Coping with uncertainty: Challenges for robust pattern formation in dynamical tissues","authors":"Tony Yu-Chen Tsai , Diana Pinheiro","doi":"10.1016/j.semcdb.2025.103629","DOIUrl":"10.1016/j.semcdb.2025.103629","url":null,"abstract":"<div><div>An outstanding question in biology is how tissue patterning emerges during development. The concept of positional information, which posits that gradients of morphogens instruct cell fate in a concentration-dependent manner, has been an influential framework to understand pattern formation. Recent studies, however, highlight that developing tissues are highly dynamic, with cellular movements, arising from local mechanical fluctuations or global morphogenetic forces, that often coincide with morphogen signaling and cell fate specification. This calls for a more dynamic understanding of pattern formation by explicitly investigating the interplay between signaling, cell fate and morphogenesis. In this review, we first discuss emerging evidence on the role of cellular movements in modulating signaling dosage and cell fate acquisition. We then examine the biophysical strategies employed by developing tissues to achieve robust patterning despite ongoing cellular dynamics and large-scale morphogenesis. While cellular movements may intuitively be viewed as disruptive to patterning programs, recent evidence suggests that when coupled with cell fate, they can act as a critical mechanism for generating and stabilizing precise tissue patterns during development.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"173 ","pages":"Article 103629"},"PeriodicalIF":6.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144572624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-04DOI: 10.1016/j.semcdb.2025.103633
Emmanuel Vikran , Tsuyoshi Hirashima
Tissue patterning during organ development consists of intricate morphogenetic processes, driven by the interplay of physical and genetic cues among constituent cells. Despite its complexity, these processes can be decomposed into fundamental morphogenetic motifs that appear repeatedly in a spatiotemporally organized manner, giving rise to diverse organ architectures. Recent studies have highlighted tissue-scale curvature as critical information for constitutive cells, which enables it to bridge mechanical and biochemical signals. In this review, we discuss the regulatory principles underlying the roles of tissue curvature in morphogenesis along with recent insights from earlier studies. Here, we focus on the dual role of tissue curvature as an instructive signal that directs collective cell behavior and as a dynamic property modulated by cellular activities. First, we introduce the concept of morphogenetic motifs and provide examples from developmental processes in various organ systems. Next, we discuss how cells collectively respond to two distinct curvature types, lateral and topographical, and examine the mechanisms by which cells sense these curvatures from a mechanobiological perspective. Finally, we highlight the repetitive terminal bifurcation in developing murine lung epithelium, illustrating how curvature-driven feedback loops, mediated through mechano-chemical multicellular couplings, ensure robust morphogenetic cycles. By integrating geometric, mechanical, and chemical cues, curvature feedback emerges as a framework for self-organized morphogenesis, providing fresh perspectives on the recurrent properties and robustness of development.
{"title":"Curvature feedback for repetitive tissue morphogenesis – Bridging algorithmic principles and self-regulatory systems","authors":"Emmanuel Vikran , Tsuyoshi Hirashima","doi":"10.1016/j.semcdb.2025.103633","DOIUrl":"10.1016/j.semcdb.2025.103633","url":null,"abstract":"<div><div>Tissue patterning during organ development consists of intricate morphogenetic processes, driven by the interplay of physical and genetic cues among constituent cells. Despite its complexity, these processes can be decomposed into fundamental morphogenetic motifs that appear repeatedly in a spatiotemporally organized manner, giving rise to diverse organ architectures. Recent studies have highlighted tissue-scale curvature as critical information for constitutive cells, which enables it to bridge mechanical and biochemical signals. In this review, we discuss the regulatory principles underlying the roles of tissue curvature in morphogenesis along with recent insights from earlier studies. Here, we focus on the dual role of tissue curvature as an instructive signal that directs collective cell behavior and as a dynamic property modulated by cellular activities. First, we introduce the concept of morphogenetic motifs and provide examples from developmental processes in various organ systems. Next, we discuss how cells collectively respond to two distinct curvature types, lateral and topographical, and examine the mechanisms by which cells sense these curvatures from a mechanobiological perspective. Finally, we highlight the repetitive terminal bifurcation in developing murine lung epithelium, illustrating how curvature-driven feedback loops, mediated through mechano-chemical multicellular couplings, ensure robust morphogenetic cycles. By integrating geometric, mechanical, and chemical cues, curvature feedback emerges as a framework for self-organized morphogenesis, providing fresh perspectives on the recurrent properties and robustness of development.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"173 ","pages":"Article 103633"},"PeriodicalIF":6.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144549554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-09-01Epub Date: 2025-07-08DOI: 10.1016/j.semcdb.2025.103628
Zimeng Wu , Mie Wong
Collective cell migration is a key tissue shaping process fundamental to development, wound healing and cancer invasion. The sensing, integration, transduction and propagation of guidance signals and the resulting generation of collective cell responses during collective cell migration can occur at several different length scales from molecular to cellular to supracellular. Furthermore, we have become aware that the cell-environment relationship during migration is bi-directional, where cells not only receive guidance cues from the environment, but also dynamically remodel the environment via their migratory behaviours. Such complex interplay of internal (i.e. intracellular) and external (i.e. cell-cell and cell-environment) interactions makes predicting the emergent output behaviours of cell groups challenging. Here, we propose a framework that combines interdisciplinary experimental and theoretical approaches to bridge the gap between molecular-level mechanisms and tissue-level phenomena during collective cell migration in complex environments. We will review recent works on both in vitro and in vivo migratory models that successfully employ some of these approaches to identify general principles explaining the input-output relationships of robustly tuneable migratory systems. By integrating in vitro with in vivo observations, we will develop more comprehensive models of how collective cell migration is orchestrated in living organisms, which will also pave the way for more effective applications in tissue engineering and disease therapeutics in the future.
{"title":"Collective cell migration across scales: A systems perspective","authors":"Zimeng Wu , Mie Wong","doi":"10.1016/j.semcdb.2025.103628","DOIUrl":"10.1016/j.semcdb.2025.103628","url":null,"abstract":"<div><div>Collective cell migration is a key tissue shaping process fundamental to development, wound healing and cancer invasion. The sensing, integration, transduction and propagation of guidance signals and the resulting generation of collective cell responses during collective cell migration can occur at several different length scales from molecular to cellular to supracellular. Furthermore, we have become aware that the cell-environment relationship during migration is bi-directional, where cells not only receive guidance cues from the environment, but also dynamically remodel the environment via their migratory behaviours. Such complex interplay of internal (i.e. intracellular) and external (i.e. cell-cell and cell-environment) interactions makes predicting the emergent output behaviours of cell groups challenging. Here, we propose a framework that combines interdisciplinary experimental and theoretical approaches to bridge the gap between molecular-level mechanisms and tissue-level phenomena during collective cell migration in complex environments. We will review recent works on both <em>in vitro</em> and <em>in vivo</em> migratory models that successfully employ some of these approaches to identify general principles explaining the input-output relationships of robustly tuneable migratory systems. By integrating <em>in vitro</em> with <em>in vivo</em> observations, we will develop more comprehensive models of how collective cell migration is orchestrated in living organisms, which will also pave the way for more effective applications in tissue engineering and disease therapeutics in the future.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"173 ","pages":"Article 103628"},"PeriodicalIF":6.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144572605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-09DOI: 10.1016/j.semcdb.2025.103621
Drishti Rajesth, Veronica Uribe , Kelly A. Smith
Gene expression in cardiac development is regulated through complex epigenetic mechanisms. Histone deacetylases (HDACs) are one of the many layers of epigenetic modulation, whereby they remove acetylation marks on histone tails, prompting chromatin tightening and therefore bring about gene repression. The most extensively characterised HDACs in cardiac development are HDACs 1–3, all belonging to the Class I HDAC family. Global as well as tissue-specific knockout models in mice have provided insight into the phenotypes generated by loss of these key molecular regulators. In some instances, molecular processes that individual HDACs regulate within cardiac development have also been revealed, although the epigenetic targets and binding partners of HDACs within cardiac development are still relatively understudied. Knowledge has also been contributed from in vitro studies using stem cell-derived models as well as burgeoning research using the zebrafish model. The aim of this review is to summarise the current knowledge of class I HDAC function during key stages of cardiac development, including cardiac specification and differentiation, looping morphogenesis, and second heart field development. The role of class I HDACs in non-cardiomyocyte populations, such as the endocardium, valves, and epicardium is also discussed.
{"title":"The open and closed case for Class I HDACs in cardiac development","authors":"Drishti Rajesth, Veronica Uribe , Kelly A. Smith","doi":"10.1016/j.semcdb.2025.103621","DOIUrl":"10.1016/j.semcdb.2025.103621","url":null,"abstract":"<div><div>Gene expression in cardiac development is regulated through complex epigenetic mechanisms. Histone deacetylases (HDACs) are one of the many layers of epigenetic modulation, whereby they remove acetylation marks on histone tails, prompting chromatin tightening and therefore bring about gene repression. The most extensively characterised HDACs in cardiac development are HDACs 1–3, all belonging to the Class I HDAC family. Global as well as tissue-specific knockout models in mice have provided insight into the phenotypes generated by loss of these key molecular regulators. In some instances, molecular processes that individual HDACs regulate within cardiac development have also been revealed, although the epigenetic targets and binding partners of HDACs within cardiac development are still relatively understudied. Knowledge has also been contributed from <em>in vitro</em> studies using stem cell-derived models as well as burgeoning research using the zebrafish model. The aim of this review is to summarise the current knowledge of class I HDAC function during key stages of cardiac development, including cardiac specification and differentiation, looping morphogenesis, and second heart field development. The role of class I HDACs in non-cardiomyocyte populations, such as the endocardium, valves, and epicardium is also discussed.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"172 ","pages":"Article 103621"},"PeriodicalIF":6.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144239566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-06-03DOI: 10.1016/j.semcdb.2025.103620
Alex M. Plum, Mattia Serra
Developmental biology has long drawn on dynamical systems to understand the diverging fates and the emerging form of the developing embryo. Cell differentiation and morphogenesis unfold in high-dimensional gene-expression spaces and position spaces. Yet, their stable and reproducible outcomes suggest low-dimensional geometric structures—e.g., fixed points, manifolds, and dynamic attracting and repelling structures—that organize cell trajectories in both spaces. This review surveys the history and recent advances in dynamical systems frameworks for development. We focus on techniques for extracting the organizing geometric structures of cell fate decisions and morphogenetic movements from experiments, as well as their interconnections. This unifying, dynamical systems perspective aids in rationalizing increasingly complex experimental datasets, facilitating principled dimensionality reduction and an integrated understanding of development, bridging typically distinct domains.
{"title":"Dynamical systems of fate and form in development","authors":"Alex M. Plum, Mattia Serra","doi":"10.1016/j.semcdb.2025.103620","DOIUrl":"10.1016/j.semcdb.2025.103620","url":null,"abstract":"<div><div>Developmental biology has long drawn on dynamical systems to understand the diverging fates and the emerging form of the developing embryo. Cell differentiation and morphogenesis unfold in high-dimensional gene-expression spaces and position spaces. Yet, their stable and reproducible outcomes suggest low-dimensional geometric structures—e.g., fixed points, manifolds, and dynamic attracting and repelling structures—that organize cell trajectories in both spaces. This review surveys the history and recent advances in dynamical systems frameworks for development. We focus on techniques for extracting the organizing geometric structures of cell fate decisions and morphogenetic movements from experiments, as well as their interconnections. This unifying, dynamical systems perspective aids in rationalizing increasingly complex experimental datasets, facilitating principled dimensionality reduction and an integrated understanding of development, bridging typically distinct domains.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"172 ","pages":"Article 103620"},"PeriodicalIF":6.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144194819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-07-02DOI: 10.1016/j.semcdb.2025.103625
Daniel B. Cortes
Modern cell and developmental biologists have access to a wide range of tools in microscopy, genetics, and molecular biology that enable the design of experiments that test hypotheses previously thought untestable or inaccessible. Still, even with the most recent advancements in technique and technology, some hypotheses remain just out of reach by in vivo and in vitro experimentation alone. Mathematical modeling is a long-standing method for the exploration of the physical sciences, chemistry and physics, and has provided significant insights into biological processes across all scales of life, from the modeling of population dynamics to the modeling of protein folding and molecular interactions. In this review, I highlight a specific subset of mathematical models – agent-based models, which explicitly simulate individual proteins or protein complexes and their physical interactions with each other within a simulated cellular environment. This review provides two specific case studies, from my own research efforts, which provide direct examples of how a cell biologist can develop mathematical models that complement their research efforts and help drive the generation of new ideas, or test hypotheses that cannot easily be tested through biological methods alone.
{"title":"A case study of agent-based modeling of cytoskeletal processes","authors":"Daniel B. Cortes","doi":"10.1016/j.semcdb.2025.103625","DOIUrl":"10.1016/j.semcdb.2025.103625","url":null,"abstract":"<div><div>Modern cell and developmental biologists have access to a wide range of tools in microscopy, genetics, and molecular biology that enable the design of experiments that test hypotheses previously thought untestable or inaccessible. Still, even with the most recent advancements in technique and technology, some hypotheses remain just out of reach by <em>in vivo</em> and <em>in vitro</em> experimentation alone. Mathematical modeling is a long-standing method for the exploration of the physical sciences, chemistry and physics, and has provided significant insights into biological processes across all scales of life, from the modeling of population dynamics to the modeling of protein folding and molecular interactions. In this review, I highlight a specific subset of mathematical models – agent-based models, which explicitly simulate individual proteins or protein complexes and their physical interactions with each other within a simulated cellular environment. This review provides two specific case studies, from my own research efforts, which provide direct examples of how a cell biologist can develop mathematical models that complement their research efforts and help drive the generation of new ideas, or test hypotheses that cannot easily be tested through biological methods alone.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"172 ","pages":"Article 103625"},"PeriodicalIF":6.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-08-01Epub Date: 2025-05-20DOI: 10.1016/j.semcdb.2025.103618
Tian Lan , Sabrina Kaminsky , Chi-Chung Wu
Somatic polyploidy, a non-inheritable form of genome multiplication, plays cell-type specific and context-dependent roles in organ development and regeneration. In the mammalian heart, embryonic cardiomyocytes are primarily diploid, which lose their ability to complete cell division and become polyploid as they mature. Unlike lower vertebrates like zebrafish, polyploid cardiomyocytes are commonly found across mammals, including humans. Intriguingly, the degree, timing, and modes of cardiomyocyte polyploidization vary greatly between species. In addition to the association with cardiomyocyte development and maturation, recent studies have established polyploidy as a barrier against cardiomyocyte proliferation and heart regeneration following cardiac injury. Hence, a thorough understanding of how and why cardiomyocyte become polyploid will provide insights into heart development and may help develop therapeutic strategies for heart regeneration. Here, we review the dynamics of cardiomyocyte polyploidization across species and how cardiomyocyte-intrinsic, -extrinsic, and environmental factors regulate this process as well as the impact of cardiomyocyte polyploidization on heart development and regeneration.
{"title":"Ploidy in cardiovascular development and regeneration","authors":"Tian Lan , Sabrina Kaminsky , Chi-Chung Wu","doi":"10.1016/j.semcdb.2025.103618","DOIUrl":"10.1016/j.semcdb.2025.103618","url":null,"abstract":"<div><div>Somatic polyploidy, a non-inheritable form of genome multiplication, plays cell-type specific and context-dependent roles in organ development and regeneration. In the mammalian heart, embryonic cardiomyocytes are primarily diploid, which lose their ability to complete cell division and become polyploid as they mature. Unlike lower vertebrates like zebrafish, polyploid cardiomyocytes are commonly found across mammals, including humans. Intriguingly, the degree, timing, and modes of cardiomyocyte polyploidization vary greatly between species. In addition to the association with cardiomyocyte development and maturation, recent studies have established polyploidy as a barrier against cardiomyocyte proliferation and heart regeneration following cardiac injury. Hence, a thorough understanding of how and why cardiomyocyte become polyploid will provide insights into heart development and may help develop therapeutic strategies for heart regeneration. Here, we review the dynamics of cardiomyocyte polyploidization across species and how cardiomyocyte-intrinsic, -extrinsic, and environmental factors regulate this process as well as the impact of cardiomyocyte polyploidization on heart development and regeneration.</div></div>","PeriodicalId":21735,"journal":{"name":"Seminars in cell & developmental biology","volume":"172 ","pages":"Article 103618"},"PeriodicalIF":6.2,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144099845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}