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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.


Related in: MedlinePlus

Expression of TFII-I in multiple tissues at E15 and E16. A. Skin and hair follicles, B. Submandibular gland, C. Dermis (E16), D. Gut Vill (E16), E-F. Skin and hair follicles and submandibular gland lacking immunoreactivity after pre-incubation of antibody with peptide. TFII-I expression is present in multiple tissues at ED15 and the immunoreactivity is completely competed by cognate peptide. TFII-I is expressed in skin and hair follicles (A) and in submandibular glands (B). Dermis demonstrates extensive immunoreactivity both in the superficial dermal layers and in underlying mesenchyme and vessels. TFII-I immunoreactivity is prominent in nucleus as well as cytoplasm in the dermis. D. Gut villi show both cytoplasmic and nuclear immunoreactivity particularly at the apical surface. Again, immunoreactivity is competed completely by pre-incubation of the antibody with peptide (E-F). Inset in Figure 5D shows nuclear and cytoplasmic locatization of TFII-I under 100 × magnification (Zeiss Axioscop, obj. Apochromat 100 ×). White arrows indicate positive reaction of specific antibody with TFII-I. Abbr.: De-Dermis, ED - Epidermis, GV-Gut Villi, SG-Submandibular Gland, VE - Vascular Endothelium
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Figure 5: Expression of TFII-I in multiple tissues at E15 and E16. A. Skin and hair follicles, B. Submandibular gland, C. Dermis (E16), D. Gut Vill (E16), E-F. Skin and hair follicles and submandibular gland lacking immunoreactivity after pre-incubation of antibody with peptide. TFII-I expression is present in multiple tissues at ED15 and the immunoreactivity is completely competed by cognate peptide. TFII-I is expressed in skin and hair follicles (A) and in submandibular glands (B). Dermis demonstrates extensive immunoreactivity both in the superficial dermal layers and in underlying mesenchyme and vessels. TFII-I immunoreactivity is prominent in nucleus as well as cytoplasm in the dermis. D. Gut villi show both cytoplasmic and nuclear immunoreactivity particularly at the apical surface. Again, immunoreactivity is competed completely by pre-incubation of the antibody with peptide (E-F). Inset in Figure 5D shows nuclear and cytoplasmic locatization of TFII-I under 100 × magnification (Zeiss Axioscop, obj. Apochromat 100 ×). White arrows indicate positive reaction of specific antibody with TFII-I. Abbr.: De-Dermis, ED - Epidermis, GV-Gut Villi, SG-Submandibular Gland, VE - Vascular Endothelium

Mentions: A survey of tissues from E15 demonstrates expression of TFII-I in multiple organ systems (Figures 3B, 4E, C, 5A-D). High levels of TFII-I expression are noted in skin and hair follicles (Figure 5A) as well as in submandibular glands (Figure 5B). Lung continues to show a similar pattern of expression to earlier time points (Figure 4E, C).


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)

Expression of TFII-I in multiple tissues at E15 and E16. A. Skin and hair follicles, B. Submandibular gland, C. Dermis (E16), D. Gut Vill (E16), E-F. Skin and hair follicles and submandibular gland lacking immunoreactivity after pre-incubation of antibody with peptide. TFII-I expression is present in multiple tissues at ED15 and the immunoreactivity is completely competed by cognate peptide. TFII-I is expressed in skin and hair follicles (A) and in submandibular glands (B). Dermis demonstrates extensive immunoreactivity both in the superficial dermal layers and in underlying mesenchyme and vessels. TFII-I immunoreactivity is prominent in nucleus as well as cytoplasm in the dermis. D. Gut villi show both cytoplasmic and nuclear immunoreactivity particularly at the apical surface. Again, immunoreactivity is competed completely by pre-incubation of the antibody with peptide (E-F). Inset in Figure 5D shows nuclear and cytoplasmic locatization of TFII-I under 100 × magnification (Zeiss Axioscop, obj. Apochromat 100 ×). White arrows indicate positive reaction of specific antibody with TFII-I. Abbr.: De-Dermis, ED - Epidermis, GV-Gut Villi, SG-Submandibular Gland, VE - Vascular Endothelium
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Expression of TFII-I in multiple tissues at E15 and E16. A. Skin and hair follicles, B. Submandibular gland, C. Dermis (E16), D. Gut Vill (E16), E-F. Skin and hair follicles and submandibular gland lacking immunoreactivity after pre-incubation of antibody with peptide. TFII-I expression is present in multiple tissues at ED15 and the immunoreactivity is completely competed by cognate peptide. TFII-I is expressed in skin and hair follicles (A) and in submandibular glands (B). Dermis demonstrates extensive immunoreactivity both in the superficial dermal layers and in underlying mesenchyme and vessels. TFII-I immunoreactivity is prominent in nucleus as well as cytoplasm in the dermis. D. Gut villi show both cytoplasmic and nuclear immunoreactivity particularly at the apical surface. Again, immunoreactivity is competed completely by pre-incubation of the antibody with peptide (E-F). Inset in Figure 5D shows nuclear and cytoplasmic locatization of TFII-I under 100 × magnification (Zeiss Axioscop, obj. Apochromat 100 ×). White arrows indicate positive reaction of specific antibody with TFII-I. Abbr.: De-Dermis, ED - Epidermis, GV-Gut Villi, SG-Submandibular Gland, VE - Vascular Endothelium
Mentions: A survey of tissues from E15 demonstrates expression of TFII-I in multiple organ systems (Figures 3B, 4E, C, 5A-D). High levels of TFII-I expression are noted in skin and hair follicles (Figure 5A) as well as in submandibular glands (Figure 5B). Lung continues to show a similar pattern of expression to earlier time points (Figure 4E, C).

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