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Originally published In Press as doi:10.1074/jbc.M302884200 on August 14, 2003
J. Biol. Chem., Vol. 278, Issue 46, 45586-45593, November 14, 2003
Expression of the Germ Cell-specific Transcription Factor ALF in Xenopus Oocytes Compensates for Translational Inactivation of the Somatic Factor TFIIA*
SangYoon Han ,
Wensheng Xie ,
Stephen R. Hammes , and
Jeff DeJong ¶
From the
Department of Molecular and Cell Biology, University of Texas at Dallas, Richardson, Texas 75080 and the Departments of Internal Medicine and Pharmacology, University of Texas Southwestern Medical School, Dallas, Texas 75390-8857
The discovery of germ cell-specific general transcription factor and coactivator variants has suggested that reproductive tissues control gene expression somewhat differently than somatic tissues. One of these factors, ALF (TFIIA ), was first described as a testis-specific counterpart of the large ( / ) subunit of TFIIA. Here we characterize endogenous ALF and TFIIA activities in the African clawed frog Xenopus laevis. ALF is present in both testis and ovary in this organism, and it completely replaces TFIIA in immature oocytes. When oocytes undergo progesterone-induced maturation, ALF activity disappears, and TFIIA activity is restored. Reactivation occurs through the translational up-regulation of two maternal TFIIA / mRNAs and involves polyadenylation of a conserved 3'-untranslated region module. The effects of ALF overexpression and ALF immunodepletion on a thymidine kinase promoter construct demonstrate that this factor serves as an active replacement for TFIIA. In contrast, overexpression of TFIIA inhibits transcription, indicating that the somatic factor fails to function properly in the context of the oocyte transcription machinery. Overall, the results show that the translationally regulated reciprocal expression of ALF and TFIIA allows for the production of an active TFIIA-like general transcription factor throughout oogenesis.
Received for publication, March 20, 2003
, and in revised form, July 16, 2003.
* This work was supported by funds from the Welch Foundation (to J. D.), the American Cancer Society (to J. D.), and the National Institutes of Health (to J. D. and to S. R. H.). 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.
¶ To whom correspondence should be addressed. Tel.: 972-883-6882; E-mail: dejong{at}utdallas.edu.

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Copyright © 2003 by the American Society for Biochemistry and Molecular Biology.
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