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Tex19.1 inhibits the N-end rule pathway and maintains acetylated SMC3 cohesin and sister chromatid cohesion in oocytes

Lookup NU author(s): Dr Lisa Ferguson, Professor Mary Herbert


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© 2020 Reichmann et al.Age-dependent oocyte aneuploidy, a major cause of Down syndrome, is associated with declining sister chromatid cohesion in postnatal oocytes. Here we show that cohesion in postnatal mouse oocytes is regulated by Tex19.1. We show Tex19.1-/- oocytes have defects maintaining chiasmata, missegregate their chromosomes during meiosis, and transmit aneuploidies to the next generation. Furthermore, we show that mouse Tex19.1 inhibits N-end rule protein degradation mediated by its interacting partner UBR2, and that Ubr2 itself has a previously undescribed role in negatively regulating the acetylated SMC3 subpopulation of cohesin in mitotic somatic cells. Lastly, we show that acetylated SMC3 is associated with meiotic chromosome axes in mouse oocytes, and that this population of cohesin is specifically depleted in the absence of Tex19.1. These findings indicate that Tex19.1 regulates UBR protein activity to maintain acetylated SMC3 and sister chromatid cohesion in postnatal oocytes and prevent aneuploidy from arising in the female germline.

Publication metadata

Author(s): Reichmann J, Dobie K, Lister LM, Crichton JH, Best D, MacLennan M, Read D, Raymond ES, Hung C-C, Boyle S, Shirahige K, Cooke HJ, Herbert M, Adams IR

Publication type: Article

Publication status: Published

Journal: Journal of Cell Biology

Year: 2020

Volume: 219

Issue: 5

Online publication date: 30/03/2020

Acceptance date: 11/02/2020

ISSN (print): 0021-9525

ISSN (electronic): 1540-8140

Publisher: Rockefeller University Press


DOI: 10.1083/jcb.201702123

PubMed id: 32232464


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