Regulation of gene expression at the beginning of mammalian development and the TEAD family of transcription factors

Kaneko, Kotaro; DePamphilis, Melvin L.

doi:10.1002/(sici)1520-6408(1998)22:1<43::aid-dvg5>3.0.co;2-7

Cited by 127 publications

(75 citation statements)

References 57 publications

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“…Thus, the L1 loop is essential for cooperative loading of TEAD to tandem sites. Earlier work by DePamphilis and coworkers (7,50) found a TEF-3 mutation (Gly-38-Asp) that renders the protein DNA-binding-deficient. In light of our findings about the L1 loop, we posit that the Asp-38 TEF-3 mutant does not bind DNA either because of (i) modified L1 structure and͞or (ii) unfavorable charge-charge interactions with DNA.…”

Section: Resultsmentioning

confidence: 99%

“…TEF-3 is found to be expressed largely in lungs and liver, but its expression also is induced by mitogenic stimulation in quiescent fibroblasts or during differentiation of myoblasts to myotubes (8). Expressed from the two-cell stage onwards, mTEAD2, hTEF-4 homolog, is sufficient for TEAD-dependent transcriptional activity during early embryonic development (7,11,12). TEF-5 is expressed in placenta and regulates human somatomammotropin gene enhancer (13,14) and influences fetal development.…”

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confidence: 99%

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Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain

Anbanandam

Albarado

Nguyen

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

117

132

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Transcription enhancer factor 1 is essential for cardiac, skeletal, and smooth muscle development and uses its N-terminal TEA domain (TEAD) to bind M-CAT elements. Here, we present the first structure of TEAD and show that it is a three-helix bundle with a homeodomain fold. Structural data reveal how TEAD binds DNA. Using structure-function correlations, we find that the L1 loop is essential for cooperative loading of TEAD molecules on to tandemly duplicated M-CAT sites. Furthermore, using a microarray chip-based assay, we establish that known binding sites of the full-length protein are only a subset of DNA elements recognized by TEAD. Our results provide a model for understanding the regulation of genome-wide gene expression during development by TEA͞ATTS family of transcription factors.DNA-binding protein ͉ gene regulation ͉ NMR structure ͉ development ͉ Scalloped

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain

Anbanandam

Albarado

Nguyen

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

117

132

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“…A mouse homologue was subsequently identified (TEAD1/TEF1; Blatt and DePamphilis, 1993;Shimizu et al, 1993), as well as three additional members of the TEAD family (TEAD2/TEF4; Jacquemin et al, 1996;Kaneko et al, 1997;Yasunami et al, 1995, TEAD3/TEF5;Kaneko et al, 1997;Yasunami et al, 1996, and TEAD4/TEF3;Jacquemin et al, 1996;Yasunami et al, 1996;Yockey et al, 1996). 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).…”

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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“…However, in morphologically arrested fertilized eggs, the major gene expression begins at the same time. Thus, this function appears to be regulated by a time-dependent biological clock (zygotic clock) (14,16,20,21). In all of these embryos, minor transcription of genes occurs during the late one-cell stage (22)(23)(24)(25)(26)(27)(28)(29)(30).…”

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confidence: 99%

“…By using the microinjection system, it has been found that although transcription can be regulated from the proximal promoter site in oocytes, fertilized eggs, and two-cell embryos, it cannot be regulated from the distal enhancer sites prior to the formation of a two-cell embryo (15,16,21,28,39,40). Previously, we observed that the exogenous transcription factor Gal4:VP16 can stimulate transcription from the proximal promoter site but not from the distal enhancer site in terminally differentiated mouse oocytes or maternal and paternal pronuclei of fertilized eggs.…”

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confidence: 99%

Lack of Enhancer Function in Mammals Is Unique to Oocytes and Fertilized Eggs

Lawinger¹,

Rastelli²,

Zhao³

et al. 1999

Journal of Biological Chemistry

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Previous studies have shown that the lack of novel coactivator activity in mouse oocytes and one-cell embryos (fertilized eggs) renders them incapable of utilizing Gal4:VP16-dependent enhancers (distal elements) but not promoters (proximal elements) in regulating transcription. This coactivator activity first appears in two-to four-cell embryos coincident with the major activation of zygotic gene expression. Here we show that whereas oocytes and fertilized eggs could utilize Sp1-dependent promoters, they could not utilize Sp1-dependent enhancers, although they showed promoter repression, which is a requirement for delineating enhancer function. In contrast, both Sp1-dependent promoters and enhancers were functional in two-to four-cell embryos. Furthermore, the same embryonic stem cell mRNA that provided the coactivator activity for Gal4: VP16-dependent enhancer function also provided Sp1-dependent enhancer function in oocytes. Therefore, the coactivator activity appears to be a requirement for general enhancer function. To determine whether the absence of enhancer function is a unique property of oocytes or a general property of other terminally differentiated cells, transcription was examined in terminally differentiated hNT neurons and their precursors, undifferentiated NT2 stem cells. The results showed that both cell types could utilize enhancers and promoters. Thus, in mammals, the lack of enhancer function appears to be unique to oocytes and fertilized eggs, suggesting that it provides a safeguard against premature activation of genes prior to zygotic gene expression during development.

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Regulation of gene expression at the beginning of mammalian development and the TEAD family of transcription factors

Cited by 127 publications

References 57 publications

Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain

Insights into transcription enhancer factor 1 (TEF-1) activity from the solution structure of the TEA domain

Transcription factor TEAD2 is involved in neural tube closure

Lack of Enhancer Function in Mammals Is Unique to Oocytes and Fertilized Eggs

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