Skip Navigation


International Immunology Advance Access originally published online on August 3, 2009
International Immunology 2009 21(9):1079-1088; doi:10.1093/intimm/dxp073
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
21/9/1079    most recent
dxp073v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Tani-ichi, S.
Right arrow Articles by Ikuta, K.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tani-ichi, S.
Right arrow Articles by Ikuta, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?


© The Japanese Society for Immunology. 2009. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Activation of the mouse TCR{gamma} enhancers by STAT5

Shizue Tani-ichi1, Masanobu Satake2 and Koichi Ikuta1

1 Laboratory of Biological Protection, Department of Biological Responses, Institute for Virus Research, Kyoto University, 53 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan
2 Department of Molecular Immunology, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryo-cho, Aoba-ku, Sendai 980-8575, Japan

Correspondence to: K. Ikuta; E-mail: ikuta{at}virus.kyoto-u.ac.jp

The IL-7R controls local accessibility of joining (J) {gamma} gene segments in the mouse TCR{gamma} locus by recruiting signal transducers and activators of transcription (STAT) 5 and transcriptional coactivators to the J{gamma} germ line promoters and inducing histone acetylation and germ line transcription. Because STAT consensus motifs are conserved not only in the J{gamma} promoters but also in the TCR{gamma} 3' enhancer (E{gamma}) elements, it is possible that STAT5 interacts with and activates E{gamma}. To address this question, we first showed that the lysine 4 residue of histone H3 is substantially methylated at E{gamma}1 and E{gamma}4 elements in wild-type early thymocytes and that the levels of the methylation are reduced in IL-7R {alpha} chain-deficient mice. We also showed that STAT5 has potential to elevate histone acetylation of the E{gamma} elements in a cytokine-dependent cell line by cytokine stimulation. Next, we demonstrated that STAT5 is recruited to the STAT consensus motifs in the E{gamma} elements after cytokine stimulation and that transcription factors Runt-related (Runx) and c-Myb are constitutively recruited to E{gamma}. Furthermore, we showed that STAT5 augments basal E{gamma} activity controlled by Runx and c-Myb. These results suggest that STAT5 is recruited to the consensus motifs in the E{gamma} elements by cytokine stimulation and augments basal E{gamma} activity independent of Runx and c-Myb. Therefore, this study implies that the E{gamma} elements might be activated in two successive steps, first by Runx and c-Myb and next by STAT5.

Keywords: {gamma}{delta} T cell, chromatin, IL-7, transcription factor

Transmitting editor: H. Karasuyama

Received 5 March 2009, accepted 7 July 2009.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.