The Role of Transcription Enhancer Factor-1 (TEF-1) Related Proteins in the Formation of M-CAT Binding Complexes in Muscle and Non-muscle Tissues

Farrance, Iain K.; Ordahl, Charles P.

doi:10.1074/jbc.271.14.8266

Cited by 60 publications

(73 citation statements)

References 54 publications

(81 reference statements)

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“…EMSAs were performed as described previously [4]. Briefly, purified TEF-1ε (50 ng), GST-TAZ-(1-239) (0.1-2 µg) or GST (5 µg) were mixed with 15000 cpm of 32 P 5 -end-labelled probe containing either a single TEF-1-binding site (CATTCCT) or containing tandem TEF-1-binding sites separated by two base pairs (MCAT1 and OGT2-56 [4]).…”

Section: Emsas (Electrophoretic Mobility-shift Assays)mentioning

confidence: 99%

“…Briefly, purified TEF-1ε (50 ng), GST-TAZ-(1-239) (0.1-2 µg) or GST (5 µg) were mixed with 15000 cpm of 32 P 5 -end-labelled probe containing either a single TEF-1-binding site (CATTCCT) or containing tandem TEF-1-binding sites separated by two base pairs (MCAT1 and OGT2-56 [4]). A 0.2 µg amount of anti-GST antibody (Amersham Biosciences) or monoclonal anti-TEF-1 antibody (Signal Transduction Laboratories) was used to supershift the protein complexes.…”

Section: Emsas (Electrophoretic Mobility-shift Assays)mentioning

confidence: 99%

“…To address this issue, we performed EMSAs, with bacterially produced and purified TEF-1ε, radiolabelled MCAT DNA probes and increasing amounts of GST-TAZ-(1-239). MCAT probes were (i) a single MCAT site, MCAT1 from the cTNT promoter, and (ii) 2 × GTIIC, which contains two MCAT sites separated by 2 bp [3,4]. TEF-1 formed a single complex with MCAT1 and two complexes with 2× GTIIC ( Figure 4A, lanes 2 and 13).…”

Section: Tef-1 and Taz Interact While Bound To Mcat Dnamentioning

confidence: 99%

“…Recently, R. Tsika and co-workers found that TEF-1 binds weakly to A/Trich binding sites in muscle promoters [2], expanding the promoters that are potentially regulated by TEF-1. The vast majority of cellular promoters that are MCAT-dependent are muscle-specific [1,[3][4][5]. In cardiac muscle, MCAT sites are also required for the full activity of promoters in the presence of hypertrophic signals [6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…In cardiac muscle, MCAT sites are also required for the full activity of promoters in the presence of hypertrophic signals [6][7][8][9]. There may be differences between TEF-1 family members, since TEF-1 and DTEF-1 are implicated in cardiac gene regulation, and RTEF-1 is involved in skeletal muscle differentiation [4,[10][11][12][13]. TEF-1 is developmentally important, since TEF-1-knockout mice die at ED (embryonic day) 10-11 from an abnormally thin heart ventricular wall [14], an MCAT site is required for PAX3 expression in the neural crest [15] and ETF-1 (TEAD2) is active in the early embryo [16].…”

Section: Introductionmentioning

confidence: 99%

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The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members

Mahoney

Hong

Yaffe

et al. 2005

Biochemical Journal

194

156

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Members of the highly related TEF-1 (transcriptional enhancer factor-1) family (also known as TEAD, for TEF-1, TEC1, ABAA domain) bind to MCAT (muscle C, A and T sites) and A/T-rich sites in promoters active in cardiac, skeletal and smooth muscle, placenta, and neural crest. TEF-1 activity is regulated by interactions with transcriptional co-factors [p160, TONDU (Vgl-1, Vestigial-like protein-1), Vgl-2 and YAP65 (Yes-associated protein 65 kDa)]. The strong transcriptional co-activator YAP65 interacts with all TEF-1 family members, and, since YAP65 is related to TAZ (transcriptional co-activator with PDZ-binding motif), we wanted to determine if TAZ also interacts with members of the TEF-1 family. In the present study, we show by GST (glutathione S-transferase) pull-down assays, by co-immunoprecipitation and by modified mammalian two-hybrid assays that TEF-1 interacts with TAZ in vitro and in vivo. Electrophoretic mobility-shift assays with purified TEF-1 and GST-TAZ fusion protein showed that TAZ interacts with TEF-1 bound to MCAT DNA. TAZ can interact with endogenous TEF-1 proteins, since exogenous TAZ activated MCAT-dependent reporter promoters. Like YAP65, TAZ interacted with all four TEF-1 family members. GST pull-down assays with increasing amounts of [ 35 S]TEF-1 and [ 35 S]RTEF-1 (related TEF-1) showed that TAZ interacts more efficiently with TEF-1 than with RTEF-1. This differential interaction also extended to the interaction of TEF-1 and RTEF-1 with TAZ in vivo, as assayed by a modified mammalian twohybrid experiment. These data show that differential association of TEF-1 proteins with transcriptional co-activators may regulate the activity of TEF-1 family members.

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Section: Emsas (Electrophoretic Mobility-shift Assays)mentioning

confidence: 99%

Section: Emsas (Electrophoretic Mobility-shift Assays)mentioning

confidence: 99%

Section: Tef-1 and Taz Interact While Bound To Mcat Dnamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members

Mahoney

Hong

Yaffe

et al. 2005

Biochemical Journal

194

156

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Precocious expression of cardiac troponin T in early chick embryos is independent of bone morphogenetic protein signaling

Antin

Bates

Zhang

et al. 2002

Developmental Dynamics

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Cardiac troponin T (cTNT) is a component of the troponin complex, which confers calcium sensitivity to contraction in skeletal and cardiac muscle. Although it is thought that most components of the contractile myofibril are expressed exclusively in differentiated muscle cells, we observed that mRNAs coding for cTNT were detectable in explanted late gastrula mesoderm at least 12 hr before cardiac myocyte differentiation. We therefore conducted a detailed analysis of cTNT gene expression in the early chick embryo. Whole-mount in situ hybridization studies showed that by Hamburger and Hamilton stage 5, cTNT mRNAs are detectable in lateral mesoderm and, by stage 6, are observed throughout the lateral embryonic and extraembryonic mesoderm in a distribution that is much broader than the recognized heart field. As myocardial cell differentiation commences, cTNT transcripts become progressively localized to the forming heart and, by stage 14, are completely restricted to heart muscle cells. Western blot analyses demonstrated that cTNT protein expression is under translational control, as cTNT protein is not detectable until stage 9, concomitant with myocardial cell differentiation. Removal of endoderm at stage 5 had no effect on cTNT mRNA levels, and the bone morphogenetic protein (BMP) inhibitor noggin failed to block cTNT expression, even in the heart-forming region and in cases where heart formation was inhibited. Implantation of noggin-expressing CHO cells at the anterior midline of stage 7 embryos resulted in cardia bifida. These findings demonstrate the precocious, BMP-independent expression of a gene coding for a myofibrillar protein and suggest that an additional regulatory pathway exists for activation of some cardiogenic genes.

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In vivo regulation of the chicken cardiac troponin T gene promoter in zebrafish embryos

Tidyman

Sehnert

Huq

et al. 2003

Developmental Dynamics

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The chicken cardiac troponin T (cTnT) gene is representative of numerous cardiac and skeletal muscle-specific genes that contain muscle-CAT (MCAT) elements within their promoters. We examined the regulation of the chicken cTnT gene in vivo in zebrafish embryos, and in vitro in cardiomyocyte, myoblast, and fibroblast cultures. Defined regions of the cTnT promoter were linked to the green fluorescent protein (GFP) gene for in vivo analysis, and the luciferase gene for in vitro analysis. Injection of the cTnT promoter constructs into fertilized zebrafish eggs resulted in GFP expression in both heart and skeletal muscle cells reproducing the pattern of expression of the endogenous cTnT gene in the chicken embryo. Promoter deletion analysis revealed that the cis-regulatory regions responsible for cardiac and skeletal muscle-specific expression functioned in an equivalent manner in both in vitro and in vivo environments. In addition, we show that mutation of the poly-ADP ribose polymerase-I (PARP-I) binding site adjacent to the distal MCAT element in the chicken cTnT promoter produced a non-cell-specific promoter in vitro and in the zebrafish. Thus, the PARP-I transcriptional regulatory mechanism that governs muscle specificity of the chicken cTnT promoter is conserved across several chordate classes spanning at least 350 million years of evolution.

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The Role of Transcription Enhancer Factor-1 (TEF-1) Related Proteins in the Formation of M-CAT Binding Complexes in Muscle and Non-muscle Tissues

Cited by 60 publications

References 54 publications

The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members

The transcriptional co-activator TAZ interacts differentially with transcriptional enhancer factor-1 (TEF-1) family members

Precocious expression of cardiac troponin T in early chick embryos is independent of bone morphogenetic protein signaling

In vivo regulation of the chicken cardiac troponin T gene promoter in zebrafish embryos

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