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Mol. Hum. Reprod. Advance Access published online on March 18, 2008
Molecular Human Reproduction, 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

Regulation of spindle and chromatin dynamics during early and late stages of oocyte maturation by aurora kinases

Jason E. Swain1,2,{dagger}, Jun Ding3, Jingwen Wu5,6 and Gary D. Smith1,2,3,4,

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

Correspondence: Gary D. Smith, 6422 Med Sci I, University of Michigan, Ann Arbor, MI 48109-0617. Telephone: 734-764-4134 Email. 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-MI transition via inhibitor ZM447439 (ZM) had no effect on germinal vesicle breakdown (GVBD). However, meiotic spindles were malformed, and microtubule organizing centers (MTOCs) 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 is regulating chromatin remodeling throughout oocyte meiosis, both pre- and post-MI.

{dagger} Current Address: Fertility Center of San Antonio, San Antonio TX 78229

Support: NIH R01 G.D.S #HD046768-01A2 and J.E.S support by T32 to G.D.S.

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


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