MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 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 Dey, A.
Right arrow Articles by Ozato, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dey, A.
Right arrow Articles by Ozato, K.

Molecular and Cellular Biology, September 2000, p. 6537-6549, Vol. 20, No. 17
0270-7306/00/$04.00+0

A Bromodomain Protein, MCAP, Associates with Mitotic Chromosomes and Affects G2-to-M Transition

Anup Dey,1 Jan Ellenberg,2,dagger Andrea Farina,1 Allen E. Coleman,3 Tetsuo Maruyama,1,Dagger Selvaggia Sciortino,1 Jennifer Lippincott-Schwartz,2 and Keiko Ozato1,*

Laboratory of Molecular Growth Regulation,1 and Cell Biology and Metabolism Branch,2 National Institute of Child Health and Human Development, and Laboratory of Genetics, Division of Basic Sciences, National Cancer Institute,3 National Institutes of Health, Bethesda, Maryland 20892-2753

Received 22 November 1999/Returned for modification 2 February 2000/Accepted 2 June 2000

We describe a novel nuclear factor called mitotic chromosome-associated protein (MCAP), which belongs to the poorly understood BET subgroup of the bromodomain superfamily. Expression of the 200-kDa MCAP was linked to cell division, as it was induced by growth stimulation and repressed by growth inhibition. The most notable feature of MCAP was its association with chromosomes during mitosis, observed at a time when the majority of nuclear regulatory factors were released into the cytoplasm, coinciding with global cessation of transcription. Indicative of its predominant interaction with euchromatin, MCAP localized on mitotic chromosomes with exquisite specificity: (i) MCAP-chromosome association became evident subsequent to the initiation of histone H3 phosphorylation and early chromosomal condensation; and (ii) MCAP was absent from centromeres, the sites of heterochromatin. Supporting a role for MCAP in G2/M transition, microinjection of anti-MCAP antibody into HeLa cell nuclei completely inhibited the entry into mitosis, without abrogating the ongoing DNA replication. These results suggest that MCAP plays a role in a process governing chromosomal dynamics during mitosis.

* Corresponding author. Mailing address: Laboratory of Molecular Growth Regulation, National Institute of Child Health and Human Development. Bldg. 6, Rm. 2A01, National Institutes of Health, Bethesda, MD 20892-2753. Phone: (301) 496-9184. Fax: (301) 480-9354. E-mail: ozatok{at}nih.gov.

dagger Present address: Gene Expression and Cell Biology/Biophysics Programmes, European Molecular Biology Laboratory, Heidelberg, Germany.

Dagger Present address: Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.

Molecular and Cellular Biology, September 2000, p. 6537-6549, Vol. 20, No. 17
0270-7306/00/$04.00+0


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 2000 by the American Society for Microbiology. All rights reserved.