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Nucleic Acids Research Advance Access originally published online on January 7, 2009
Nucleic Acids Research 2009 37(4):1061-1072; doi:10.1093/nar/gkn1036
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Nucleic Acids Research, 2009, Vol. 37, No. 4 1061-1072
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.


Gene regulation, Chromatin and Epigenetics

The Torso signaling pathway modulates a dual transcriptional switch to regulate tailless expression

Yu-Chien Chen1, Suewei I. Lin1, Ying-Kuan Chen1, Chuen-Sheue Chiang2 and Gwo-Jen Liaw1,*

1Department of Life Sciences and Institute of Genome Sciences, National Yang-Ming University, Taipei, 112 Taiwan and 2Centers for Disease Control, Department of Health, Taipei, 115 Taiwan, ROC

*To whom correspondence should be addressed. Tel: +886 2 2826 7232; Fax: +886 2 2820 2449; Email: gjliaw{at}ym.edu.tw

Received July 15, 2008. Revised November 13, 2008. Accepted December 14, 2008.

The Torso (Tor) signaling pathway activates tailless (tll) expression by relieving tll repression. None of the repressors identified so far, such as Capicuo, Groucho and Tramtrack69 (Ttk69), bind to the tor response element (tor-RE) or fully elucidate tll repression. In this study, an expanded tll expression pattern was shown in embryos with reduced heat shock factor (hsf) and Trithorax-like (Trl) activities. The GAGA factor, GAF encoded by Trl, bound weakly to the tor-RE, and this binding was enhanced by both Hsf and Ttk69. A similar extent of expansion of tll expression was observed in embryos with simultaneous knockdown of hsf, Trl and ttk69 activities, and in embryos with constitutively active Tor. Hsf is a substrate of mitogen-activated protein kinase and S378 is the major phosphorylation site. Phosphorylation converts Hsf from a repressor to an activator that works with GAF to activate tll expression. In conclusion, the GAF/Hsf/Ttk69 complex binding to the tor-RE remodels local chromatin structure to repress tll expression and the Tor signaling pathway activate tll expression by modulating a dual transcriptional switch.


Present address: Suewei I. Lin, Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA


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