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Peer-reviewedCC BY 4.0The EMBO Journal

Reciprocal coupling between EMT and BMP morphogen signalling drives collective cell invasion

  • Yuri Takahashi1
  • Alexandra Neaverson1
  • Lara Busby1,2
  • Filip Twarowski1
  • Carlos Camacho-Macorra1
  • Guillermo Serrano Nájera1
  • Benjamin Steventon1
  1. 1Department of Genetics, University of Cambridge, Cambridge, CB2 3EH UK
  2. 2Present Address: University of California, Berkeley, CA USA
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Abstract

During collective cell invasion, epithelial-to-mesenchymal transition (EMT) and morphogen signalling-mediated cell fate specification are traditionally viewed as a linear cascade: morphogens drive cell fates that activate EMT gene expression programs. Here, we uncover reciprocal coupling between EMT initiation and BMP signalling mediated by SNAI2 and SMAD1. Using ex vivo chick tissue explants, we demonstrate that substrate-induced migration upregulates SMAD1 expression, activating BMP signalling across germ layers. Single-cell RNA sequencing reveals SNAI2 and SMAD1 co-expression in EMT initiation regions, and SNAI2 overexpression is sufficient to induce ectopic SMAD1 expression in vivo. Ex vivo CRISPR-Cas9 experiments further demonstrate that SNAI2 is required for SMAD1 expression and BMP signalling. While BMP signalling is dispensable for EMT initiation, it regulates cell fate proportions, dispersal dynamics, precursor region depletion rates, and migration directionality. This coupling provides a mechanism for synchronising cell fate specification with invasion progression during axis elongation, positioning SNAI2-SMAD1 interaction as mechanism to coordinate cell fate specification and EMT during collective cell invasion.

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Cite

BibTeXRIS
BibTeX
@article{takahashi2026reciprocal,
  title = {{Reciprocal coupling between EMT and BMP morphogen signalling drives collective cell invasion}},
  author = {Yuri Takahashi and Alexandra Neaverson and Lara Busby and Filip Twarowski and Carlos Camacho-Macorra and Guillermo Serrano Nájera and Benjamin Steventon},
  journal = {The EMBO Journal},
  year = {2026},
  month = oct,
  doi = {10.1038/s44318-026-00916-8},
  url = {https://doi.org/10.1038/s44318-026-00916-8},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Reciprocal coupling between EMT and BMP morphogen signalling drives collective cell invasion
AU  - Yuri Takahashi
AU  - Alexandra Neaverson
AU  - Lara Busby
AU  - Filip Twarowski
AU  - Carlos Camacho-Macorra
AU  - Guillermo Serrano Nájera
AU  - Benjamin Steventon
PY  - 2026
DA  - 2026/10/07
JO  - The EMBO Journal
DO  - 10.1038/s44318-026-00916-8
UR  - https://doi.org/10.1038/s44318-026-00916-8
AB  - During collective cell invasion, epithelial-to-mesenchymal transition (EMT) and morphogen signalling-mediated cell fate specification are traditionally viewed as a linear cascade: morphogens drive cell fates that activate EMT gene expression programs. Here, we uncover reciprocal coupling between EMT initiation and BMP signalling mediated by SNAI2 and SMAD1. Using ex vivo chick tissue explants, we demonstrate that substrate-induced migration upregulates SMAD1 expression, activating BMP signalling across germ layers. Single-cell RNA sequencing reveals SNAI2 and SMAD1 co-expression in EMT initiation regions, and SNAI2 overexpression is sufficient to induce ectopic SMAD1 expression in vivo. Ex vivo CRISPR-Cas9 experiments further demonstrate that SNAI2 is required for SMAD1 expression and BMP signalling. While BMP signalling is dispensable for EMT initiation, it regulates cell fate proportions, dispersal dynamics, precursor region depletion rates, and migration directionality. This coupling provides a mechanism for synchronising cell fate specification with invasion progression during axis elongation, positioning SNAI2-SMAD1 interaction as mechanism to coordinate cell fate specification and EMT during collective cell invasion.
SN  - 0261-4189
SN  - 1460-2075
ER  -