RT Journal Article SR Electronic T1 Tex19.1 Regulates Acetylated SMC3 Cohesin and Prevents Aneuploidy in Mouse Oocytes JF bioRxiv FD Cold Spring Harbor Laboratory SP 102285 DO 10.1101/102285 A1 Judith Reichmann A1 Karen Dobie A1 Lisa M. Lister A1 Diana Best A1 James H. Crichton A1 Marie MacLennan A1 David Read A1 Eleanor S. Raymond A1 Chao-Chun Hung A1 Shelagh Boyle A1 Katsuhiko Shirahige A1 Howard J. Cooke A1 Wendy A. Bickmore A1 Mary Herbert A1 Ian R. Adams YR 2017 UL http://biorxiv.org/content/early/2017/02/07/102285.abstract AB 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 that Tex19.1-/- oocytes have defects in the maintenance of chiasmata, mis-segregate their chromosomes during meiosis, and transmit aneuploidies to the next generation. By reconstituting aspects of this pathway in mitotic somatic cells, we show that Tex19.1 regulates an acetylated SMC3-marked subpopulation of cohesin by inhibiting the activity of the E3 ubiquitin ligase UBR2 towards specific substrates, and that UBR2 itself has a previously undescribed role in negatively regulating acetylated SMC3. Lastly, we show that acetylated SMC3 is associated with meiotic chromosome axes in oocytes, but that this is reduced in the absence of Tex19.1. These findings indicate that Tex19.1 maintains acetylated SMC3 and sister chromatid cohesion in postnatal oocytes, and prevents aneuploidy in the female germline.