HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 280, Issue 26, 24957-24967, July 1, 2005

This Article Full Text Full Text (PDF) All Versions of this Article: 280/26/24957    most recent M414437200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Philipova, R. Articles by Whitaker, M. Search for Related Content PubMed PubMed Citation Articles by Philipova, R. Articles by Whitaker, M. Social Bookmarking                      What's this?

Inhibiting MAP Kinase Activity Prevents Calcium Transients and Mitosis Entry in Early Sea Urchin Embryos^*

Rada Philipova, Mark G. Larman, Calum P. Leckie, Patrick K. Harrison, Laurence Groigno, and Michael Whitaker

From the Institute of Cell and Molecular Biosciences, Faculty of Medical Sciences, University of Newcastle upon Tyne, NE2 4HH, United Kingdom

A transient calcium increase triggers nuclear envelope breakdown (mitosis entry) in sea urchin embryos. Cdk1/cyclin B kinase activation is also known to be required for mitosis entry. More recently, MAP kinase activity has also been shown to increase during mitosis. In sea urchin embryos, both kinases show a similar activation profile, peaking at the time of mitosis entry. We tested whether the activity of both kinases is required for mitosis entry and whether either kinase controls mitotic calcium signals. We found that reducing the activity of either mitotic kinase prevents nuclear envelope breakdown, despite the presence of a calcium transient, when cdk1/cyclin B kinase activity is alone inhibited. When MAP kinase activity alone was inhibited, the calcium signal was absent, suggesting that MAP kinase activity is required to generate the calcium transient that triggers nuclear envelope breakdown. However, increasing intracellular free calcium by microinjection of calcium buffers or InsP₃ while MAP kinase was inhibited did not itself induce nuclear envelope breakdown, indicating that additional MAP kinase-regulated events are necessary. After MAP kinase inhibition early in the cell cycle, the early events of the cell cycle (pronuclear migration/fusion and DNA synthesis) were unaffected, but chromosome condensation and spindle assembly are prevented. These data indicate that in sea urchin embryos, MAP kinase activity is part of a signaling complex alongside two components previously shown to be essential for entry into mitosis: the calcium transient and the increase in cdk1/cyclinB kinase activity.

Received for publication, December 22, 2004 , and in revised form, April 19, 2005.

^* This work was supported by the Wellcome Trust. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed. Tel.: 44-191-222-5264; Fax: 44-191-222-5164; E-mail: michael.whitaker{at}ncl.ac.uk.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				W. L. Zhang, P. Huitorel, A.-M. Geneviere, S. Chiri, and B. Ciapa Inactivation of MAPK in mature oocytes triggers progression into mitosis via a Ca2+-dependent pathway but without completion of S phase J. Cell Sci., September 1, 2006; 119(17): 3491 - 3501. [Abstract] [Full Text] [PDF]

				M. Whitaker Calcium at Fertilization and in Early Development Physiol Rev, January 1, 2006; 86(1): 25 - 88. [Abstract] [Full Text] [PDF]