Coupling of cell proliferation to the segmentation clock promotes robust somite scaling
8 affiliations
- 1Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences), University Medical Center Utrecht, Utrecht, the Netherlands
- 2Hubrecht Institute
- 3Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Wilberforce Road, Cambridge CB3 0WA, UK; Institute of Science and Technology Austria (ISTA), 3400 Klosterneuburg, Austria
- 4University of Cambridge, IST Austria
- 5University of Cambridge
- 6UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK
- 7Department of Applied Mathematics and Theoretical Physics, Centre for Mathematical Sciences, University of Cambridge, Wilberforce Road, Cambridge CB3 0WA, UK; Gurdon Institute, University of Cambridge, Tennis Court Road, Cambridge CB2 1QN, UK; Cambridge Stem Cell Institute, Jeffrey Cheah Biomedical Centre, University of Cambridge, Cambridge CB2 0AW, UK
- 8Hubrecht Institute-KNAW (Royal Netherlands Academy of Arts and Sciences), University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address: [email protected]
Abstract
While scaling developmental processes is fundamental to maintaining robust tissue patterning, the mechanisms underlying this process are enigmatic. Somitogenesis, the periodic segmentation of growing mesodermal tissue in vertebrate embryos 1 , involves precise scaling with the unsegmented presomitic mesoderm (PSM) over developmental time and under perturbation 2–4 . Somitogenesis is spatiotemporally regulated by FGF and Wnt morphogen gradients and the segmentation clock — oscillations in Notch, Wnt, and FGF signalling 5–7 . Here, we find that cell proliferation is distributed throughout the oscillating PSM. Long-term single-cell tracking in mouse embryo tails uncovered a correlation between cell cycle progression and the segmentation clock, with microfluidics-based entrainment indicating coupling between the cell cycle and signalling oscillations, likely through S-phase inducing Cyclins. A theoretical model suggests this coupling ensures uniform PSM growth, uniform morphogen dilution and precise somite formation, which we validated experimentally by blocking cell proliferation. Our findings reveal that coupling cell proliferation to signalling oscillations is crucial for robust somitogenesis and precise somite scaling.
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BibTeX
@article{oostrom2026coupling,
title = {{Coupling of cell proliferation to the segmentation clock promotes robust somite scaling}},
author = {Marek J. van Oostrom and Yuting I. Li and Wilke H. M. Meijer and Tomas E. J. C. Noordzij and Charis Fountas and Erika Timmers and Jeroen Korving and Wouter M. Thomas and Dimitri Fabrèges and Andrew J. Copp and Benjamin D. Simons and Katharina F. Sonnen},
journal = {Developmental Cell},
year = {2026},
month = nov,
doi = {10.1016/j.devcel.2026.10.005},
url = {https://doi.org/10.1016/j.devcel.2026.10.005},
note = {CC BY},
}
RIS
TY - JOUR
TI - Coupling of cell proliferation to the segmentation clock promotes robust somite scaling
AU - Marek J. van Oostrom
AU - Yuting I. Li
AU - Wilke H. M. Meijer
AU - Tomas E. J. C. Noordzij
AU - Charis Fountas
AU - Erika Timmers
AU - Jeroen Korving
AU - Wouter M. Thomas
AU - Dimitri Fabrèges
AU - Andrew J. Copp
AU - Benjamin D. Simons
AU - Katharina F. Sonnen
PY - 2026
DA - 2026/11/01
JO - Developmental Cell
DO - 10.1016/j.devcel.2026.10.005
UR - https://doi.org/10.1016/j.devcel.2026.10.005
AB - While scaling developmental processes is fundamental to maintaining robust tissue patterning, the mechanisms underlying this process are enigmatic. Somitogenesis, the periodic segmentation of growing mesodermal tissue in vertebrate embryos 1 , involves precise scaling with the unsegmented presomitic mesoderm (PSM) over developmental time and under perturbation 2–4 . Somitogenesis is spatiotemporally regulated by FGF and Wnt morphogen gradients and the segmentation clock — oscillations in Notch, Wnt, and FGF signalling 5–7 . Here, we find that cell proliferation is distributed throughout the oscillating PSM. Long-term single-cell tracking in mouse embryo tails uncovered a correlation between cell cycle progression and the segmentation clock, with microfluidics-based entrainment indicating coupling between the cell cycle and signalling oscillations, likely through S-phase inducing Cyclins. A theoretical model suggests this coupling ensures uniform PSM growth, uniform morphogen dilution and precise somite formation, which we validated experimentally by blocking cell proliferation. Our findings reveal that coupling cell proliferation to signalling oscillations is crucial for robust somitogenesis and precise somite scaling.
SN - 1534-5807
SN - 1878-1551
ER -