Abstract:
:The high incidence of aneuploidy in the embryo is considered the principal cause for low human fecundity. However, the prevalence of aneuploidy dramatically declines as pregnancy progresses, with the steepest drop occurring as the embryo completes implantation. Despite the fact that the plasticity of the embryo in dealing with aneuploidy is fundamental to normal development, the mechanisms responsible for eliminating aneuploid cells are unclear. Here, using a mouse model of chromosome mosaicism, we show that aneuploid cells are preferentially eliminated from the embryonic lineage in a p53-dependent process involving both autophagy and apoptosis before, during and after implantation. Moreover, we show that diploid cells in mosaic embryos undertake compensatory proliferation during the implantation stages to confer embryonic viability. Together, our results indicate a close link between aneuploidy, autophagy, and apoptosis to refine the embryonic cell population and ensure only chromosomally fit cells proceed through development of the fetus.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Singla S,Iwamoto-Stohl LK,Zhu M,Zernicka-Goetz Mdoi
10.1038/s41467-020-16796-3subject
Has Abstractpub_date
2020-06-11 00:00:00pages
2958issue
1issn
2041-1723pii
10.1038/s41467-020-16796-3journal_volume
11pub_type
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