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J. Biol. Chem., Vol. 278, Issue 47, 46523-46532, November 21, 2003

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The T-box Factor Tpit Recruits SRC/p160 Co-activators and Mediates Hormone Action^*

Mario Maira, Catherine Couture, Gwendal Le Martelot, Anne-Marie Pulichino, Steve Bilodeau, and Jacques Drouin

From the Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal, 110, avenue des Pins Ouest, Montréal, Québec H2W 1R7, Canada and the Université de Montréal, Département de Biochimie, C.P. 6128, Succursale Centre-ville, Montréal, Québec H3C 3J7, Canada

Tpit (Tbx19) is a transcription factor belonging to the T-box family, and it is essential for late differentiation of pituitary pro-opiomelanocortin (POMC)-expressing corticotroph and melanotroph cells. Tpit is also required, both in humans and mice, for cell-specific expression of the POMC gene in cooperation with the homeoprotein Pitx1. Despite their important roles as developmental regulators, the molecular mechanisms underpinning the functions of T-box factors in general, and of Tpit in particular, are still poorly defined. We now report that Tpit functions as an activator of transcription by recruiting SRC/p160 co-activators to its cognate DNA target in the POMC promoter, the Tpit/Pitx-RE. We also show that Tpit is a mediator of hormone signaling and that the Tpit/Pitx-RE is responsive to signals elicited by hypothalamic corticotropin-releasing hormone. These signals are mediated by the cAMP-dependent protein kinase and mitogen-activated protein kinase pathways, and activation of cAMP-dependent protein kinase also enhances Tpit and SRC-dependent transcription. We have previously shown that corticotropin-releasing hormone action is also exerted at the POMC promoter through the orphan nuclear receptor NGFI-B and its recruitment of SRC co-activators. Given that Tpit exhibits transcriptional synergy with NGFI-B, our results suggest that Tpit, along with NGFI-B and SRC-2, is part of a transcription regulatory complex assembled on the POMC promoter in response to hormonal stimulation.

Received for publication, May 29, 2003 , and in revised form, September 10, 2003.

^* This work was funded by the Canadian Institutes of Health Research. 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.

Recipient of a doctoral research award from the Canadian Institutes of Health Research.

To whom correspondence should be addressed: Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal, 110, avenue des Pins Ouest, Montréal, PQ H2W 1R7, Canada. Tel.: 514-987-5680; Fax: 514-987-5575; E-mail: drouinj{at}ircm.qc.ca.

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