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

Fijalkowska I, Sharma D, Bult CJ, Danoff SK - BMC Res Notes (2010)

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Johns Hopkins University School of Medicine, Department of Medicine, Cardiopulmonary and Critical Care Division, 1830 E, Monument Street, Baltimore, MD 21205, USA. sdanoff@jhmi.edu.

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.

No MeSH data available.


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Liver at E11 (A, C) and at E15 (B, D). A. TFII-I is present in a principally cytoplasmic distribution in liver. B. Sections through lung (Lu), diaphragm (Di) and liver (Li) demonstrate differential levels of TFII-I expression, with higher levels in lung and diaphragm than in liver. C and D. Immunoreactivity is competed completely by pre-incubation of the antibody with peptide. Abbr.: Di - Diaphragm, HPC-Hepatic Primordial Cells, Li - Liver, Lu - Lungs,
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Figure 3: Liver at E11 (A, C) and at E15 (B, D). A. TFII-I is present in a principally cytoplasmic distribution in liver. B. Sections through lung (Lu), diaphragm (Di) and liver (Li) demonstrate differential levels of TFII-I expression, with higher levels in lung and diaphragm than in liver. C and D. Immunoreactivity is competed completely by pre-incubation of the antibody with peptide. Abbr.: Di - Diaphragm, HPC-Hepatic Primordial Cells, Li - Liver, Lu - Lungs,

Mentions: Sections through liver (Figure 3A) show widespread, low-level expression of TFII-I in developing hepatocytes. This immunoreactivity is fully blocked by pre-incubation of the antibody with peptide as described in methods (Figure 3C, D).


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

Fijalkowska I, Sharma D, Bult CJ, Danoff SK - BMC Res Notes (2010)

Liver at E11 (A, C) and at E15 (B, D). A. TFII-I is present in a principally cytoplasmic distribution in liver. B. Sections through lung (Lu), diaphragm (Di) and liver (Li) demonstrate differential levels of TFII-I expression, with higher levels in lung and diaphragm than in liver. C and D. Immunoreactivity is competed completely by pre-incubation of the antibody with peptide. Abbr.: Di - Diaphragm, HPC-Hepatic Primordial Cells, Li - Liver, Lu - Lungs,
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2921380&req=5

Figure 3: Liver at E11 (A, C) and at E15 (B, D). A. TFII-I is present in a principally cytoplasmic distribution in liver. B. Sections through lung (Lu), diaphragm (Di) and liver (Li) demonstrate differential levels of TFII-I expression, with higher levels in lung and diaphragm than in liver. C and D. Immunoreactivity is competed completely by pre-incubation of the antibody with peptide. Abbr.: Di - Diaphragm, HPC-Hepatic Primordial Cells, Li - Liver, Lu - Lungs,
Mentions: Sections through liver (Figure 3A) show widespread, low-level expression of TFII-I in developing hepatocytes. This immunoreactivity is fully blocked by pre-incubation of the antibody with peptide as described in methods (Figure 3C, D).

Bottom Line: 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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Johns Hopkins University School of Medicine, Department of Medicine, Cardiopulmonary and Critical Care Division, 1830 E, Monument Street, Baltimore, MD 21205, USA. sdanoff@jhmi.edu.

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.

No MeSH data available.


Related in: MedlinePlus