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Analysis of TATA-binding protein 2 (TBP2) and TBP expression suggests different roles for the two proteins in regulation of gene expression during oogenesis and early mouse development

Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), UMR 7104, CNRS, INSERM, ULP, BP 10142, CU de Strasbourg, 67404 Illkirch Cedex, France and ¹ Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas, TX77030, USA

Correspondence should be addressed to M E Torres-Padilla; Email: metp{at}igbmc.u-strasbg.fr or L Tora; Email: laszlo{at}igbmc.u-strasbg.fr

Gametogenesis, the process during which germ cells are generated is essential for reproduction. In mammals, maternal mRNA and proteins present in the oocyte are required to ensure the progression of development until the embryo activates its genome after fertilisation. It is well established that the oocyte synthesises these maternal factors during oocyte growth and then undergoes a quiescent transcriptional period that will be resumed only after fertilisation. However, the mechanisms that govern transcriptional regulation and subsequent silencing during oogenesis are not well understood. Here, we have examined the expression and localisation of the TATA-binding protein (TBP) and the related protein TBP2 (also called TRF3, TBP-related factor 3) during oogenesis and in early mouse embryos. We show that TBP is expressed in the oocytes at the beginning of folliculogenesis, but it is undetectable during further stages of oocyte development, and becomes abundant again only after fertilisation. In contrast to TBP, we found that TBP2 is highly expressed in growing oocytes during folliculogenesis, declines upon ovulation, and is almost undetectable after fertilisation by the two-cell stage. The mirroring localisation profile of TBP and TBP2 suggests different roles for the two proteins in establishing specialised programs of gene expression during oocyte development and in early mouse embryos. Analysis of mutant mouse ovaries in which oocyte-specific factors have been knocked-out suggests that TBP2 is a potential candidate for regulating transcriptional control of oogenesis. Moreover, our results obtained with oocytes lacking the oocyte-specific nuclear chaperone nucleoplasmin 2 suggest that TBP2 function may be related to non-condensed chromatin conformation.

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