Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 10 December 2002
Vol. 2002, Issue 162, p. tw468
[DOI: 10.1126/stke.2002.162.tw468]


DEVELOPMENT From General to Specific

In vitro studies and work done in yeast have suggested that the transcription factor DRAP1 functions as a "general" transcriptional regulator that represses transcription by preventing the interaction of TFIIB with TBP (the TATA box-binding protein of TFIIB). Iratni et al. examined the function of DRAP1during early mouse development and found that the mutant embryo exhibited gastrulation defects consistent with increased activity of Nodal, a secreted morphogen of the transforming growth factor-β family that is the primary inducer of mesoderm during gastrulation. Nodal signaling is inhibited in the early embryo by DRAP1, most likely through its interaction with FoxH1. Thus, a factor that was previously thought to be a general transcriptional regulator displays a specific role in embryonic patterning through the regulation of Nodal's positive feedback loop, providing a mechanism for regulation of morphogen signaling.

R. Iratni, Y.-T. Yan, C. Chen, J. Ding, Y. Zhang, S. M. Price, D. Reinberg, M. M. Shen, Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1. Science 298, 1996-1999 (2002). [Abstract] [Full Text]

Citation: From General to Specific. Sci. STKE 2002, tw468 (2002).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882