TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm

Vassilev, Alex; Kaneko, Kotaro J.; Shu, Hongjun; Zhao, Yingming; DePamphilis, Melvin L.

doi:10.1101/gad.888601

Cited by 632 publications

(591 citation statements)

References 35 publications

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“…Overexpression of Merlin promotes phosphorylation and nuclear extrusion of YAP, a downstream target of the Hippo kinase cascade [33,94], which functions as a co-activator of TEAD transcription factors (Fig 3B; [97,98]). By contrast, silencing of Merlin induces TEAD-dependent transcription [92].…”

Section: Activation Of the Hippo Pathwaymentioning

confidence: 99%

Merlin: a tumour suppressor with functions at the cell cortex and in the nucleus

et al. 2012

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Inhibition of proliferation by cell-to-cell contact is essential for tissue organization, and its disruption contributes to tumorigenesis. The FERM domain protein Merlin, encoded by the NF2 tumour suppressor gene, is an important mediator of contact inhibition. Merlin was thought to inhibit mitogenic signalling and activate the Hippo pathway by interacting with diverse target-effectors at or near the plasma membrane. However, recent studies highlight that Merlin pleiotropically affects signalling by migrating into the nucleus and inducing a growth-suppressive programme of gene expression through its direct inhibition of the CRL4 DCAF1 E3 ubiquitin ligase. In addition, Merlin promotes the establishment of epithelial adhesion and polarity by recruiting Par3 and aPKC to E-cadherin-dependent junctions, and by ensuring the assembly of tight junctions. These recent advances suggest that Merlin acts at the cell cortex and in the nucleus in a similar, albeit antithetic, manner to the oncogene β-catenin.

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Section: Activation Of the Hippo Pathwaymentioning

confidence: 99%

Merlin: a tumour suppressor with functions at the cell cortex and in the nucleus

et al. 2012

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“…These transcription factors are defined by the presence of the 72 amino acid TEA DNA binding domain in their N-terminal half that is virtually identical among TEAD proteins and by the conspicuous homology among their C-terminal halves (Kaneko and DePamphilis, 1998). This conservation of structure is reflected in the ability of these proteins to bind the same transcriptional coactivator proteins (Mahoney et al, 2005;Vassilev et al, 2001) and to substitute for TEAD proteins in other organisms (Deshpande et al, 1997). Nevertheless, despite their structural similarities, the four mammalian TEAD proteins are not functionally redundant, because mice lacking TEAD1 fail to develop a proper heart and die between embryonic day 11 (E11) and E12 (Chen et al, 1994), whereas mice lacking TEAD4 arrest development before E3.5 (Yagi et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Transcription factor TEAD2 is involved in neural tube closure

Kaneko

Kohn

Liu

et al. 2007

Genesis

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Summary-TEAD2, one of the first transcription factors expressed at the beginning of mammalian development, appears to be required during neural development. For example, Tead2 expression is greatest in the dorsal neural crest where it appears to regulate expression of Pax3, a gene essential for brain development. Consistent with this hypothesis, we found that inactivation of the Tead2 gene in mice significantly increased the risk of exencephaly (a defect in neural tube closure). However, none of the embryos exhibited spina bifida, the major phenotype of Pax3 nullizygous embryos, and expression of Pax3 in E11.5 Tead2 nullizygous embryos was normal. Thus, Tead2 plays a role in neural tube closure that is independent of its putative role in Pax3 regulation. In addition, the risk of exencephaly was greatest with Tead2 nullizygous females, and could be suppressed either by folic acid or pifithrin-α. These results reveal a maternal genetic contribution to neural tube closure, and suggest that Tead2-deficient mice provide a model for anencephaly, a common human birth defect that can be prevented by folic acid. genesis 45:577-587, 2007.

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“…Class 1: interacting proteins with co-activation function [p160 steroid hormone receptor co-activators and YAP65 (Yes-associated protein 65 kDa)]. These TEF-1 co-factors contain transactivation domains, interact with TEF-1 and activate transcription of MCATdependent promoters ( [22][23][24], and see below). Class 2: interacting proteins without co-activation function [TONDU (Vgl-1, Vestigial-like protein-1), Vgl-2 and Vgl-3].…”

Section: Introductionmentioning

confidence: 99%

“…YAP65 and TAZ also have similar domain structures; one or two WW domains, a 14-3-3-binding site and a C-terminal PDZ-binding motif [23]. Phosphorylated YAP65 and TAZ are bound to the phospho-serine/threoninebinding protein 14-3-3 in the cytoplasm, and dephosphorylated YAP65 and TAZ are found in the nucleus, where they function as transcriptional co-activators [23,24]. Intracellular localization of YAP65 can be regulated by overexpression of Akt/protein kinase B [35].…”

Section: Introductionmentioning

confidence: 99%

“…YAP65 and TAZ are transcriptional co-activators for a number of transcription factors: p63/p73 [36], the TEF-1 gene family [24], the ErbB4 nuclear fragment [37], Runx2/Cbfa1 [38] and TTF-1/ Nkx2.1 [39]. YAP65/TAZ-interacting transcription factors have diverse functions, including cell-cycle regulation, pro-and antiapoptosis, DNA repair, skeletal muscle and osteoblast differentiation, cardiac trabeculae and conduction system development, and thyroid-and lung-specific gene expression.…”

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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TEAD/TEF transcription factors utilize the activation domain of YAP65, a Src/Yes-associated protein localized in the cytoplasm

Cited by 632 publications

References 35 publications

Merlin: a tumour suppressor with functions at the cell cortex and in the nucleus

Merlin: a tumour suppressor with functions at the cell cortex and in the nucleus

Transcription factor TEAD2 is involved in neural tube closure

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

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