P53 and mTOR signalling determine fitness selection through cell competition during early mouse embryonic development

Sarah Bowling, Aida Gregorio, Margarida Sancho, Sara Pozzi, Marieke Aarts, Massimo Signore, Michael Schneider, Juan Pedro Martinez-Barbera, Jesús Gil () and Tristan A. Rodríguez ()
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Sarah Bowling: Hammersmith Hospital Campus
Aida Gregorio: Hammersmith Hospital Campus
Margarida Sancho: Hammersmith Hospital Campus
Sara Pozzi: Newlife Birth Defects Research Centre
Marieke Aarts: MRC London Institute of Medical Sciences (LMS)
Massimo Signore: Newlife Birth Defects Research Centre
Michael Schneider: Hammersmith Hospital Campus
Juan Pedro Martinez-Barbera: Newlife Birth Defects Research Centre
Jesús Gil: MRC London Institute of Medical Sciences (LMS)
Tristan A. Rodríguez: Hammersmith Hospital Campus

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: Abstract Ensuring the fitness of the pluripotent cells that will contribute to future development is important both for the integrity of the germline and for proper embryogenesis. Consequently, it is becoming increasingly apparent that pluripotent cells can compare their fitness levels and signal the elimination of those cells that are less fit than their neighbours. In mammals the nature of the pathways that communicate fitness remain largely unknown. Here we identify that in the early mouse embryo and upon exit from naive pluripotency, the confrontation of cells with different fitness levels leads to an inhibition of mTOR signalling in the less fit cell type, causing its elimination. We show that during this process, p53 acts upstream of mTOR and is required to repress its activity. Finally, we demonstrate that during normal development around 35% of cells are eliminated by this pathway, highlighting the importance of this mechanism for embryonic development.

Date: 2018
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DOI: 10.1038/s41467-018-04167-y

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