Journal
NATURE CELL BIOLOGY
Volume 16, Issue 1, Pages 27-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb2881
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Funding
- Max Planck Society
- European Research Council under the European Commission
- Stem Cell Network North Rhine Westphalia
- German Research Foundation (Deutsche Forschungsgemeinschaft)
- World Premier International Research Japan
- National Institutes of Health (NIH) [NIH RO1-HD052115, RO1-DK084391]
- NYSTEM
- European Commission
- Naito
- Uehara Memorial Foundation
- Marie Curie FP7 IIF fellowship [273193]
- Grants-in-Aid for Scientific Research [24681039] Funding Source: KAKEN
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R01HD052115] Funding Source: NIH RePORTER
- NATIONAL CANCER INSTITUTE [P30CA008748] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK084391] Funding Source: NIH RePORTER
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It is now recognized that extensive expression heterogeneities among cells precede the emergence of lineages in the early mammalian embryo. To establish a map of pluripotent epiblast (EPI) versus primitive endoderm (PrE) lineage segregation within the inner cell mass (ICM) of the mouse blastocyst, we characterized the gene expression profiles of individual ICM cells. Clustering analysis of the transcriptomes of 66 cells demonstrated that initially they are non-distinguishable. Early in the segregation, lineage-specific marker expression exhibited no apparent correlation, and a hierarchical relationship was established only in the late blastocyst. Fgf4 exhibited a bimodal expression at the earliest stage analysed, and in its absence, the differentiation of PrE and EPI was halted, indicating that Fgf4 drives, and is required for, ICM lineage segregation. These data lead us to propose a model where stochastic cell-to-cell expression heterogeneity followed by signal reinforcement underlies ICM lineage segregation by antagonistically separating equivalent cells.
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