MCB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Other Versions of this Article:
MCB.01661-06v1
27/4/1254    most recent
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 Google Scholar
Google Scholar
Right arrow Articles by Inai, T.
Right arrow Articles by Tsuchiya, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Inai, T.
Right arrow Articles by Tsuchiya, E.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, February 2007, p. 1254-1263, Vol. 27, No. 4
0270-7306/07/$08.00+0     doi:10.1128/MCB.01661-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Interplay between Chromatin and trans-Acting Factors on the IME2 Promoter upon Induction of the Gene at the Onset of Meiosis{triangledown}

Tomomi Inai,{dagger} Masashi Yukawa,{dagger} and Eiko Tsuchiya*

Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Kagamiyama, Higashi-Hiroshima 739-8530, Japan

Received 6 September 2006/ Returned for modification 4 October 2006/ Accepted 30 November 2006

The IME2 gene is one of the key regulators of the initiation of meiosis in budding yeast. This gene is repressed during mitosis through the repressive chromatin structure at the promoter, which is maintained by the Rpd3-Sin3 histone deacetylase (HDAC) complex. IME2 expression in meiosis requires Gcn5/histone acetyltransferase, the transcriptional activator Ime1, and the chromatin remodeler RSC; however, the molecular basis of IME2 activation had not been previously defined. We found that, during mitotic growth, a nucleosome masked the TATA element of IME2, and this positioning depended on HDAC. This chromatin structure was remodeled at meiosis by RSC that was recruited to TATA by Ime1. Stable tethering of Ime1 to the promoter required the presence of Gcn5. Interestingly, Ime1 binding to the promoter was kept at low levels during the very early stages in meiosis, even when the levels of Ime1 and histone H3 acetylation at the promoter were at their highest, making a 4- to 6-h delay of the IME2 expression from that of IME1. HDAC was continuously present at the promoter regardless of the transcriptional condition of IME2, and deletion of RPD3 allowed the IME2 expression shortly after the expression of IME1, suggesting that HDAC plays a role in regulating the timing of IME2 expression.


* Corresponding author. Mailing address: Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Kagamiyama, Higashi-Hiroshima 739-8530, Japan. Phone and fax: 81 82 424 7868. E-mail: etsuchi{at}hiroshima-u.ac.jp.

{triangledown} Published ahead of print on 11 December 2006.

{dagger} T.I. and M.Y. contributed equally to this work.


Molecular and Cellular Biology, February 2007, p. 1254-1263, Vol. 27, No. 4
0270-7306/07/$08.00+0     doi:10.1128/MCB.01661-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.







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 © 2007 by the American Society for Microbiology. All rights reserved.