BMP signalling is required for extra-embryonic ectoderm development during pre-to-post-implantation transition of the mouse embryo
Abstract
At implantation, the mouse embryo undergoes a critical transformation which requires the precise spatiotemporal control of signalling pathways necessary for morphogenesis and developmental progression. The role played by such signalling pathways during this transition are largely unexplored, due to the inaccessibility of the embryo during the implantation when it becomes engulfed by uterine tissues. Genetic studies demonstrate that mutant embryos for BMPs die around gastrulation. Here we have aimed to dissect the role of BMPs during pre-to post-implantation transition by using a protocol permitting the development of the embryo beyond implantation stages in vitro and using stem cells to mimic post-implantation tissue organisation. By assessing both the canonical and non-canonical mechanisms of BMP, we show that the loss of canonical BMP activity compromises the extra-embryonic ectoderm development. Our analyses demonstrate that BMP signalling maintains stem cell populations within both embryonic/extra-embryonic tissues during pre-to post-implantation development. These results may provide insight into the role played by BMP signalling in controlling early embryogenesis.
Additional Information
© 2020 Published by Elsevier Inc. Received 7 May 2020, Revised 6 November 2020, Accepted 8 November 2020, Available online 17 November 2020. We thank colleagues in the M.Z.G. laboratory for insightful comments. We are grateful to Andy Cox for critical reading of the manuscript and drawing models in Figs. 1A and 2E. The M.Z.G. laboratory is supported by grants from the European Research Council (669198); the Wellcome Trust (098287/Z/12/Z). B.S. is grateful to Yale School of Medicine for start-up funding and also supported by the International Research Fellowship Program 2214/A from Scientific and Technological Research Council of Turkey, and the Akdeniz University Scientific Research Fund (Project No: TDK-2015-1109). Author contributions: Conceptualization: B.S., M.Z-G.; Methodology & Investigation: B.S. Writing: B.S, M.Z-G.; Supervision: N.D., M.Z-G. Funding: B.S., N.D., M.Z.-G. The authors declare no competing or financial interests.Attached Files
Accepted Version - nihms-1715009.pdf
Supplemental Material - 1-s2.0-S0012160620302979-mmc1.docx
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Additional details
- PMCID
- PMC8219371
- Eprint ID
- 106701
- Resolver ID
- CaltechAUTHORS:20201117-110225184
- European Research Council (ERC)
- 669198
- Wellcome Trust
- 098287/Z/12/Z
- Yale School of Medicine
- Türkiye Bilimsel ve Teknolojik Araştırma Kurumu (TÜBİTAK)
- 2214/A
- Akdeniz Üniversitesi
- TDK-2015-1109
- Created
-
2020-11-17Created from EPrint's datestamp field
- Updated
-
2023-07-17Created from EPrint's last_modified field
- Caltech groups
- Division of Biology and Biological Engineering (BBE)