This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yamamoto, T. M.
Right arrow Articles by Maller, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yamamoto, T. M.
Right arrow Articles by Maller, J. L.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, June 2008, p. 4196-4203, Vol. 28, No. 12
0270-7306/08/$08.00+0     doi:10.1128/MCB.00169-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Regulation of the Aurora B Chromosome Passenger Protein Complex during Oocyte Maturation in Xenopus laevis{triangledown}

Tomomi M. Yamamoto, Andrea L. Lewellyn, and James L. Maller*

Howard Hughes Medical Institute and Department of Pharmacology, University of Colorado School of Medicine, Aurora, Colorado 80045

Received 1 February 2008/ Returned for modification 25 February 2008/ Accepted 21 March 2008

The dynamics of the Aurora B protein kinase during Xenopus oocyte meiotic maturation were examined. Resting G2 oocytes express inactive Aurora B that is not associated with other subunits of the chromosome passenger complex (CPC). Activity increases near the time of germinal vesicle breakdown in progesterone-treated oocytes, and this increase is correlated with the synthesis of inner centromere protein (INCENP) and survivin, components of the CPC. Ablation of INCENP synthesis led to the failure of progesterone treatment to activate Aurora B, but biochemical progression through the meiosis I-to-II transition and arrest at metaphase II were not affected. At fertilization, Aurora B was deactivated in concert with the degradation of INCENP, and the levels of Aurora B kinase activity and INCENP oscillated in subsequent embryonic cell cycles. Prevention of the decrease in Aurora B activity at fertilization by expression of ectopic wild-type INCENP, but not kinase-dead Aurora B INCENP, blocked calcium-induced exit from metaphase arrest in egg extracts.


* Corresponding author. Mailing address: Howard Hughes Medical Institute and Department of Pharmacology, University of Colorado School of Medicine, Aurora, CO 80045. Phone: (303) 724-1673. Fax: (303) 724-1626. E-mail: Jim.Maller{at}uchsc.edu

{triangledown} Published ahead of print on 31 March 2008.


Molecular and Cellular Biology, June 2008, p. 4196-4203, Vol. 28, No. 12
0270-7306/08/$08.00+0     doi:10.1128/MCB.00169-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

  • Pascreau, G., Eckerdt, F., Lewellyn, A. L., Prigent, C., Maller, J. L. (2009). Phosphorylation of p53 Is Regulated by TPX2-Aurora A in Xenopus Oocytes. J. Biol. Chem. 284: 5497-5505 [Abstract] [Full Text]