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The transcription factor SOX17 is involved in the transcriptional control of the uteroglobin gene in rabbit endometrium

✍ Scribed by Carlos Garcia; Enrique Calvo; Antonio Nieto

Publisher
John Wiley and Sons
Year
2007
Tongue
English
Weight
249 KB
Volume
102
Category
Article
ISSN
0730-2312

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✦ Synopsis

Abstract

The transcription of the uteroglobin gene (ug) is induced by progesterone in the rabbit endometrium, primarily through the binding of the progesterone receptor to the distal region of the ug promoter. However, other transcription factors participate in the progesterone action. The proximal ug promoter contains several putative consensus sequences for the binding of various progesterone‐dependent endometrial nuclear factors (Perez Martinez et al. [1996] Arch Biochem Biophys 333: 12–18), suggesting that several transcription factors might be implicated in the hormonal induction of ug. We report here that one of these progesterone‐dependent factors specifically binds to the sequence CACAATG (−183/−177) of the rabbit ug promoter. This sequence (hereafter called element G′) is very similar to the consensus sequence for binding of the SOX family of transcription factors. Mutation of the element G′ reduced transcription from the ug promoter in transient expression experiments. The endometrial factor was purified and analyzed by nano‐liquid chromatography and ion trap coupled mass spectrometry yielding two partial amino acid sequences corresponding to a region of SOX17 that is highly conserved inter‐species. This identification was confirmed by immunological techniques using a specific anti‐SOX17 antibody. In agreement with the above findings, overexpression of SOX17 in transfected endometrial cells increased transcription from the ug promoter. SOX17 gradually accumulated in the nucleus in vivo concomitant with the induction of ug expression by progesterone in the endometrium. Thus, these findings implicate, for the first time, SOX17 in the transcriptional control of rabbit ug. J. Cell. Biochem. 102: 665–679, 2007. © 2007 Wiley‐Liss, Inc.

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