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Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition.

Publication ,  Journal Article
Tang, W; Wu, JQ; Guo, Y; Hansen, DV; Perry, JA; Freel, CD; Nutt, L; Jackson, PK; Kornbluth, S
Published in: Molecular biology of the cell
August 2008

The transition of oocytes from meiosis I (MI) to meiosis II (MII) requires partial cyclin B degradation to allow MI exit without S phase entry. Rapid reaccumulation of cyclin B allows direct progression into MII, producing a cytostatic factor (CSF)-arrested egg. It has been reported that dampened translation of the anaphase-promoting complex (APC) inhibitor Emi2 at MI allows partial APC activation and MI exit. We have detected active Emi2 translation at MI and show that Emi2 levels in MI are mainly controlled by regulated degradation. Emi2 degradation in MI depends not on Ca(2+)/calmodulin-dependent protein kinase II (CaMKII), but on Cdc2-mediated phosphorylation of multiple sites within Emi2. As in MII, this phosphorylation is antagonized by Mos-mediated recruitment of PP2A to Emi2. Higher Cdc2 kinase activity in MI than MII allows sufficient Emi2 phosphorylation to destabilize Emi2 in MI. At MI anaphase, APC-mediated degradation of cyclin B decreases Cdc2 activity, enabling Cdc2-mediated Emi2 phosphorylation to be successfully antagonized by Mos-mediated PP2A recruitment. These data suggest a model of APC autoinhibition mediated by stabilization of Emi2; Emi2 proteins accumulate at MI exit and inhibit APC activity sufficiently to prevent complete degradation of cyclin B, allowing MI exit while preventing interphase before MII entry.

Duke Scholars

Published In

Molecular biology of the cell

DOI

EISSN

1939-4586

ISSN

1059-1524

Publication Date

August 2008

Volume

19

Issue

8

Start / End Page

3536 / 3543

Related Subject Headings

  • Proto-Oncogene Proteins c-mos
  • Neutrophils
  • Models, Biological
  • Mice, Inbred C57BL
  • Mice
  • Meiosis
  • Leukocytes
  • Humans
  • HL-60 Cells
  • Gene Expression Regulation
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Tang, W., Wu, J. Q., Guo, Y., Hansen, D. V., Perry, J. A., Freel, C. D., … Kornbluth, S. (2008). Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition. Molecular Biology of the Cell, 19(8), 3536–3543. https://doi.org/10.1091/mbc.e08-04-0417
Tang, Wanli, Judy Qiju Wu, Yanxiang Guo, David V. Hansen, Jennifer A. Perry, Christopher D. Freel, Leta Nutt, Peter K. Jackson, and Sally Kornbluth. “Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition.Molecular Biology of the Cell 19, no. 8 (August 2008): 3536–43. https://doi.org/10.1091/mbc.e08-04-0417.
Tang W, Wu JQ, Guo Y, Hansen DV, Perry JA, Freel CD, et al. Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition. Molecular biology of the cell. 2008 Aug;19(8):3536–43.
Tang, Wanli, et al. “Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition.Molecular Biology of the Cell, vol. 19, no. 8, Aug. 2008, pp. 3536–43. Epmc, doi:10.1091/mbc.e08-04-0417.
Tang W, Wu JQ, Guo Y, Hansen DV, Perry JA, Freel CD, Nutt L, Jackson PK, Kornbluth S. Cdc2 and Mos regulate Emi2 stability to promote the meiosis I-meiosis II transition. Molecular biology of the cell. 2008 Aug;19(8):3536–3543.

Published In

Molecular biology of the cell

DOI

EISSN

1939-4586

ISSN

1059-1524

Publication Date

August 2008

Volume

19

Issue

8

Start / End Page

3536 / 3543

Related Subject Headings

  • Proto-Oncogene Proteins c-mos
  • Neutrophils
  • Models, Biological
  • Mice, Inbred C57BL
  • Mice
  • Meiosis
  • Leukocytes
  • Humans
  • HL-60 Cells
  • Gene Expression Regulation