Email updates

Keep up to date with the latest news and content from BMC Research Notes and BioMed Central.

Open Access Short Report

Expression of the transcription factor, TFII-I, during post-implantation mouse embryonic development

Iwona Fijalkowska1, Deva Sharma1, Carol J Bult2 and Sonye K Danoff1*

Author Affiliations

1 Johns Hopkins University School of Medicine, Department of Medicine, Cardiopulmonary and Critical Care Division, 1830 E. Monument Street, Baltimore, MD 21205, USA

2 The Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA

For all author emails, please log on.

BMC Research Notes 2010, 3:203  doi:10.1186/1756-0500-3-203

Published: 20 July 2010

Abstract

Background

General transcription factor (TFII-I) is a multi-functional transcription factor encoded by the Gtf2i gene, that has been demonstrated to regulate transcription of genes critical for development. Because of the broad range of genes regulated by TFII-I as well as its potential role in a significant neuro-developmental disorder, developing a comprehensive expression profile is critical to the study of this transcription factor. We sought to define the timing and pattern of expression of TFII-I in post-implantation embryos at a time during which many putative TFII-I target genes are expressed.

Findings

Antibodies to the N-terminus of TFII-I were used to probe embryonic mouse sections. TFII-I protein is widely expressed in the developing embryo. TFII-I is expressed throughout the period from E8-E16. However, within this period there are striking shifts in localization from cytoplasmic predominant to nuclear. TFII-I expression varies in both a spatial and temporal fashion. There is extensive expression in neural precursors at E8. This expression persists at later stages. TFII-I is expressed in developing lung, heart and gut structures. There is no evidence of isoform specific expression. Available data regarding expression patterns at both an RNA and protein level throughout development are also comprehensively reviewed.

Conclusions

Our immunohistochemical studies of the temporal and spatial expression patterns of TFII-I in mouse embryonic sections are consistent with the hypothesis that hemizygous deletion of GTF2I in individuals with Williams-Beuren Syndrome contributes to the distinct cognitive and physiological symptoms associated with the disorder.