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  The BCL-2 pathway preserves mammalian genome integrity by eliminating recombination-defective oocytes

ElInati, E., Zielinska, A., McCarthy, A., Kubikova, N., Maciulyte, V., Mahadevaiah, S., et al. (2020). The BCL-2 pathway preserves mammalian genome integrity by eliminating recombination-defective oocytes. Nature Communications, 11: 2598. doi:10.1038/s41467-020-16441-z.

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 Creators:
ElInati, E., Author
Zielinska, A.1, Author           
McCarthy, A., Author
Kubikova, N., Author
Maciulyte, V., Author
Mahadevaiah, S., Author
Sangrithi, M. N., Author
Ojarikre, O., Author
Wells, D., Author
Niakan, K. K., Author
Schuh, M.1, Author           
Turner, J. M. A., Author
Affiliations:
1Department of Meiosis, MPI for Biophysical Chemistry, Max Planck Society, ou_2205654              

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Free keywords: Developmental biology; Embryogenesis; Genetics; Germline development; Oogenesis
 Abstract: DNA double-strand breaks (DSBs) are toxic to mammalian cells. However, during meiosis, more than 200 DSBs are generated deliberately, to ensure reciprocal recombination and orderly segregation of homologous chromosomes. If left unrepaired, meiotic DSBs can cause aneuploidy in gametes and compromise viability in offspring. Oocytes in which DSBs persist are therefore eliminated by the DNA-damage checkpoint. Here we show that the DNA-damage checkpoint eliminates oocytes via the pro-apoptotic BCL-2 pathway members Puma, Noxa and Bax. Deletion of these factors prevents oocyte elimination in recombination-repair mutants, even when the abundance of unresolved DSBs is high. Remarkably, surviving oocytes can extrude a polar body and be fertilised, despite chaotic chromosome segregation at the first meiotic division. Our findings raise the possibility that allelic variants of the BCL-2 pathway could influence the risk of embryonic aneuploidy.

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Language(s): eng - English
 Dates: 2020-05-25
 Publication Status: Published online
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41467-020-16441-z
 Degree: -

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Title: Nature Communications
Source Genre: Journal
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Pages: 10 Volume / Issue: 11 Sequence Number: 2598 Start / End Page: - Identifier: -