ArticleNature communications2019
In vivo topology converts competition for cell-matrix adhesion into directional migration.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Tissue flow acts as a guidance cue for immune cell polarization and directional migration.Nature cell biology · 2026Article
- Long-range chemical signalling in vivo is regulated by mechanical signals.Nature materials · 2026Article
- Collective migration modes in development, tissue repair and cancer.Nature reviews. Molecular cell biology · 2025Review
- Stretch-induced endogenous electric fields drive directed collective cell migration in vivo.Nature materials · 2025Article
- The influence of SDF-1 (CXCL12) gene in health and disease: a review of literature.Biophysical reviews · 2025Review
- Polarity and migration of cranial and cardiac neural crest cells: underlying molecular mechanisms and disease implications.Frontiers in cell and developmental biology · 2024Review
- Cell-matrix and cell-cell interaction mechanics in guiding migration.Biochemical Society transactions · 2023Review
- Paracrine regulation of neural crest EMT by placodal MMP28.PLoS biology · 2023Article
- The Tumor SuppressorJournal of developmental biology · 2023Article
- Unravelling cell migration: defining movement from the cell surface.Cell adhesion & migration · 2022Review
- Durotaxis: the mechanical control of directed cell migration.The FEBS journal · 2022Review
- The mechanical forces that shape our senses.Development (Cambridge, England) · 2022Review
- Viscoelasticity, Like Forces, Plays a Role in Mechanotransduction.Frontiers in cell and developmental biology · 2022Review
- Emerging concepts on the mechanical interplay between migrating cells and microenvironmentFrontiers in cell and developmental biology · 2022Review
- The mechanosensitive channel Piezo1 cooperates with semaphorins to control neural crest migration.Development (Cambridge, England) · 2021Article
- Physiological electric fields induce directional migration of mammalian cranial neural crest cells.Developmental biology · 2021Article
- Filopodia-based contact stimulation of cell migration drives tissue morphogenesis.Nature communications · 2021Article
- Dynamic expression of MMP28 during cranial morphogenesis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Epithelial-to-mesenchymal transition and different migration strategies as viewed from the neural crest.Current opinion in cell biology · 2020Review
- The extracellular matrix in development.Development (Cambridge, England) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When migrating in vivo, cells are exposed to numerous conflicting signals: chemokines, repellents, extracellular matrix, growth factors. The roles of several of these molecules have been studied individually in vitro or in vivo, but we have yet to understand how cells integrate them. To start addressing this question, we used the cephalic neural crest as a model system and looked at the roles of its best examples of positive and negative signals: stromal-cell derived factor 1 (Sdf1/Cxcl12) and class3-Semaphorins. Here we show that Sdf1 and Sema3A antagonistically control cell-matrix adhesion via opposite effects on Rac1 activity at the single cell level. Directional migration at the population level emerges as a result of global Semaphorin-dependent confinement and broad activation of adhesion by Sdf1 in the context of a biased Fibronectin distribution. These results indicate that uneven in vivo topology renders the need for precise distribution of secreted signals mostly dispensable.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.