Redundant Roles of <i>Tead1</i> and <i>Tead2</i> in Notochord Development and the Regulation of Cell Proliferation and Survival

Sawada, Atsushi; Kanazawa, Hiroshi; Ukita, Kanako; Nishioka, Noriyuki; Imuta, Yu; Sasaki, Hiroshi

doi:10.1128/mcb.01759-07

Cited by 164 publications

(157 citation statements)

References 72 publications

(86 reference statements)

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“…The TEAD family of transcription factors, of which TEAD1 is the best characterised, regulate growth and differentiation in many tissues. This is exemplified by an important role for TEAD1 in embryonic development (Sawada et al, 2008;Zhang et al, 2008). TEAD1 binds several co-activators to stimulate the transcription of target genes (Gupta et al, 1997(Gupta et al, , 2001).…”

Section: Discussionmentioning

confidence: 99%

TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer

et al. 2008

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Prostate cancer is the most frequently diagnosed male cancer, and its clinical outcome is difficult to predict. The disease may involve the inappropriate expression of genes that normally control the proliferation of epithelial cells in the basal layer and their differentiation into luminal cells. Our aim was to identify novel basal cell markers and assess their prognostic and functional significance in prostate cancer. RNA from basal and luminal cells isolated from benign tissue by immunoguided laser-capture microdissection was subjected to expression profiling. We identified 112 and 267 genes defining basal and luminal populations, respectively. The transcription factor TEAD1 and the ubiquitin ligase c-Cbl were identified as novel basal cell markers. Knockdown of either marker using siRNA in prostate cell lines led to decreased cell growth in PC3 and disrupted acinar formation in a 3D culture system of RWPE1. Analyses of prostate cancer tissue microarray staining established that increased protein levels of either marker were associated with decreased patient survival independent of other clinicopathological metrics. These data are consistent with basal features impacting on the development and clinical course of prostate cancers.

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Section: Discussionmentioning

confidence: 99%

TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer

et al. 2008

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“…Tead2-VP16 and Yap1 regulated largely overlapping sets of genes. However, only a few of the Tead/Yap1-regulated genes in NIH3T3 cells were affected in Tead1 Milewski et al, 2004;Nishioka et al, 2008;Sawada et al, 2008;Sawada et al, 2005;Yagi et al, 2007). Our recent study on Tead1;Tead2 double-mutant embryos revealed the genetic interactions between Tead1/2 and Yap1 during embryogenesis, and their necessity in cell proliferation and apoptosis .…”

Section: Mitsunori Ota and Hiroshi Sasaki*mentioning

confidence: 99%

Mammalian Tead proteins regulate cell proliferation and contact inhibition as transcriptional mediators of Hippo signaling

Ota¹,

Sasaki²

2008

Development

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-/-embryos. Most of the previously identified Yap1-regulated genes were not affected in NIH3T3 cells or mutant mice. In embryos, levels of nuclear Yap1 and Tead1 varied depending on cell type. Strong nuclear accumulation of Yap1 and Tead1 were seen in myocardium, correlating with requirements of Tead1 for proliferation. However, their distribution did not always correlate with proliferation. Taken together, mammalian Tead proteins regulate cell proliferation and contact inhibition as a transcriptional mediator of Hippo signaling, but the mechanisms by which Tead/Yap1 regulate cell proliferation differ depending on the cell type, and Tead, Yap1 and Hippo signaling may play multiple roles in mouse embryos.

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“…TEAD factors clearly have redundant functions in vivo, as while TEAD2 knockout mice have only a minor phenotype, TEAD1/TEAD2 double-knockout mice have pleiotropic abnormalities that are much more severe than the loss of TEAD1 or TEAD2 alone. 8,34 Cell-specific regulation of proliferation genes by TEAD factors. In non-muscle cells, TEAD factors promote proliferation via Ctgf or Ccnd1.…”

Section: Tead4 Regulates Myoblast Differentiationmentioning

confidence: 99%

Transcription factor TEAD4 regulates expression of Myogenin and the unfolded protein response genes during C2C12 cell differentiation

Benhaddou

Keime

et al. 2011

Cell Death Differ

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The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA-binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy among the family members. Expression of the TEA/ATTS DNA-binding domain that acts as a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, whereas selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation. RNA-seq identifies a set of genes whose expression is strongly reduced upon TEAD4 knockdown among which are structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF (connective tissue growth factor) to promote differentiation. Together these results show that TEAD factor activity is essential for normal C2C12 cell differentiation and suggest a role for TEAD4 in regulating expression of the unfolded protein response genes. The TEAD transcription factors make a highly conserved family of 4 DNA-binding proteins 1,2 containing the TEA (Yeast (TEC-1), Aspergillus nidulans (AbaA) and Drosophilla (scalloped))/ATTS (Aspergillus nidulans (AbaA), Yeast (TEC-1), human TEF1, and Drosophilla (scalloped)) DNA-binding domain (DBD). 3,4 The TEA domain comprises a three-helix bundle with a homeodomain fold and binds a consensus MCAT (5 0 -CATTCCA/ T-3 0 ) element originally defined as the GT-II motif of the simian virus 40 (SV40) enhancer. 5 Mammalian TEADs are widely expressed with prominent expression in the nervous system and muscle. In-vitro, cell-based, knockout and transgenic studies have addressed the role of TEAD factors in regulation of muscle-expressed genes. 6-8 Cardiac troponin T, myosin, heavy polypeptide 7, cardiac muscle, beta (b-MHC) and Myocardin, have functional MCAT motifs in their regulatory regions. 2 Stimulation of a1-adrenergic signalling has been shown to induce cardiac hypertrophy and activate transcription of the b-MHC and skeletal a-actin genes in an MCAT-and TEAD-dependent manner in cultured neonatal rat cardiomyocytes. 9 Cardiac muscle-specific overexpression of TEAD4 in transgenic mice has been shown to induce arhythmias in vivo. 8 TEAD4 is specifically expressed in developing skeletal muscle in mouse embryos. 1 Chromatin immunoprecipitation-array hybridization (ChIP-chip) showed that TEAD4 is a direct target of the MYOD1 and MYOG transcription factors in C2C12 cells. 10 Although TEAD4 upregulation by MYOD1 and MYOG during differentiation is thought to activate transcription of muscle structural genes, mouse knockouts do not show any evident role for TEAD4 i...

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Redundant Roles of Tead1 and Tead2 in Notochord Development and the Regulation of Cell Proliferation and Survival

Cited by 164 publications

References 72 publications

TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer

TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer

Mammalian Tead proteins regulate cell proliferation and contact inhibition as transcriptional mediators of Hippo signaling

Transcription factor TEAD4 regulates expression of Myogenin and the unfolded protein response genes during C2C12 cell differentiation

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