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Mol. Hum. Reprod. Advance Access originally published online on March 18, 2008
Molecular Human Reproduction 2008 14(5):291-299; doi:10.1093/molehr/gan015
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© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
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Regulation of spindle and chromatin dynamics during early and late stages of oocyte maturation by aurora kinases

Jason E. Swain1,2,7, Jun Ding3, Jingwen Wu4,5 and Gary D. Smith1,2,3,6,8

1Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA 2Reproductive Sciences Program, University of Michigan, Ann Arbor, MI 48109, USA 3Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, MI 48109, USA 4Department of Histology and Embryology, Shanghai Jiaotong University School of Medicine, Shanghai 200025, People’s Republic of China 5Shanghai Key Laboratory for Reproductive Medicine, Shanghai Jiaotong University School of Medicine, Shanghai 200025, People’s Republic of China 6Department of Urology, University of Michigan, Ann Arbor, MI 48109, USA

8 Correspondence address. 6422 Med Sci I, University of Michigan, Ann Arbor, MI 48109-0617, USA.Tel: +1-734-764-4134; E-mail: smithgd{at}umich.edu

Examination of factors regulating oocyte chromatin remodeling is crucial to circumvent embryonic aneuploidy and resulting defects. Aurora kinases (AURK) are involved in regulation of chromatin remodeling, however, little attention has been paid to AURKs in regard to oocyte maturation. Meiotically incompetent mouse oocytes contain transcripts for all three Aurk isoforms: A, B and C. Upon achieving meiotic competence, oocytes showed significant increases in transcript levels of all three Aurk isoforms and transcript levels remained unchanged as oocytes progressed through meiosis, with AurkA being the predominant isoform. Inhibition of oocyte AURKs during the prophase–metaphase I (MI) transition via inhibitor ZM447439 (ZM) had no effect on germinal vesicle breakdown. However, meiotic spindles were malformed, and microtubule organizing centers and chromatin were scattered. Chromosomal spreads of MI oocytes indicated AURK inhibition resulted in abnormal chromosome condensation. Furthermore, inhibition of AURK during prophase I–MII prevented completion of MII and extrusion of the polar body. Inhibition of AURKs during the MI–MII transition resulted in significantly fewer cells progressing to MII and induced aberrant chromatin remodeling. Further analysis indicated that inhibition of AURKs resulted in absence of histone-H3 phosphorylation at serine 10 and 28. These data suggest a ZM-sensitive AURK may be an oocyte histone-H3 kinase capable of regulating chromatin remodeling throughout oocyte meiosis, both pre- and post-MI.

Key words: chromosomal disorders/meiosis/oocyte/signal transduction/kinase

7 Present address: Fertility Center of San Antonio, San Antonio, TX 78229, USA

Submitted on January 29, 2008; resubmitted on February 29, 2008; accepted on March 12, 2008.


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