![]() 1999) and in cardiac muscle ( Azakie et al. TEAD-3/TEF-5 is expressed primarily in the placenta ( Jacquemin et al. 2000), TEAD-4/TEF-3 appears to play a specific role in activating skeletal muscle genes ( Jacquemin et al. 1997 Butler and Ordahl 1999 Ueyama et al. Although TEAD-1/TEF-1 is required for gene expression in cardiac muscle ( Chen et al. Moreover, disruption of the TEAD-1/TEF-1 gene prevents heart biogenesis during mouse development, arguing that TEAD gene functions are not redundant ( Chen et al. 1998), suggesting that each protein has a unique function. However, each protein exhibits different expression patterns with respect to tissue and developmental stage specificity ( Kaneko et al. ![]() At least one TEAD gene is expressed in most adult tissues, and all four are abundantly expressed in some tissues, such as lung ( Yockey et al. Because these proteins share in common the TEA DNA binding domain, we refer to them as TEA domain (TEAD) proteins to avoid ambiguity with acronyms for other proteins. 1988), and later recognized as a family of four ubiquitous and highly conserved transcription factors found in mammals, birds, fungi, flies, and yeast ( Kaneko and DePamphilis 1998 Jacquemin et al. Transcription enhancer factor-1 (TEF-1) was first cloned in human cells as an activator of the simian virus 40 (SV40) enhancer ( Davidson et al. Because TEAD-dependent transcription was limited by YAP65, and YAP65 also binds Src/Yes protein tyrosine kinases, we propose that YAP65 regulates TEAD-dependent transcription in response to mitogenic signals. However, whereas TEAD was concentrated in the nucleus, excess YAP65 accumulated in the cytoplasm as a complex with the cytoplasmic localization protein, 14-3-3. Therefore, the carboxy-terminal acidic activation domain in YAP is the transcriptional activation domain for TEAD transcription factors. Conversely, TEAD overexpression squelched YAP activity. Expression of YAP in lymphocytic cells that normally do not support TEAD-dependent transcription (e.g., MPC11) resulted in up to 300-fold induction of TEAD activity. Both this interaction and sequence-specific DNA binding by TEAD were required for transcriptional activation in mouse cells. ![]() YAP65 interacted specifically with the carboxyl terminus of all four TEAD proteins. TEAD-2/TEF-4 protein purified from mouse cells was associated predominantly with a novel TEAD-binding domain at the amino terminus of YAP65, a powerful transcriptional coactivator. Mammals express four highly conserved TEAD/TEF transcription factors that bind the same DNA sequence, but serve different functions during development. ![]()
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