The N Termini of Friend of GATA (FOG) Proteins Define a Novel Transcriptional Repression Motif and a Superfamily of Transcriptional Repressors

Lin, Andy; Roche, Andrea E.; Wilk, Jeannine; Svensson, E. C.

doi:10.1074/jbc.m411240200

Cited by 63 publications

(70 citation statements)

References 46 publications

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“…In vitro studies have shown that GATA-4 (or the closely related factors GATA-5 and -6) can bind and trans-activate several genes expressed in differentiating and terminally differentiated members of the parietal and zymogenic cell lineages (Tamura et al, 1993;Mushiake et al, 1994;Nishi et al, 1997;Sakamoto et al, 1998Sakamoto et al, , 2000, and studies with chimeric mice underscore the in vivo contributions of GATA-4 to expression of these genes (Jacobsen et al, 2002). In vitro, FOGs can either enhance or repress the activity of GATA-4, depending on the promoter studied (Lu et al, 1999;Viger, 2001, 2003;Lin et al, 2004). Gata4 ki/ki distal gastric epithelium exhibits augmented expression of Shh, suggesting that GATA-4:FOG interaction plays a direct or indirect role in limiting the expression of this factor.…”

Section: Discussionmentioning

confidence: 99%

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

Jacobsen¹,

Mannisto²,

Porter-Tinge³

et al. 2005

Developmental Dynamics

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Transcription factor GATA-4 is a key participant in cytodifferentiation of the mouse hindstomach. Here we show that GATA-4 cooperates with a Friend-of-GATA (FOG) cofactor to direct gene expression in this segment of gut. Immunohistochemical staining revealed that GATA-4 and FOG-1 are co-expressed in hindstomach epithelial cells from embryonic days (E) 11.5 to 18.5. The other member of the mammalian FOG family, FOG-2, was not detected in gastric epithelium. To show that GATA-4:FOG interactions influence stomach development, we analyzed Gata4 ki/ki mice, which express a mutant GATA-4 that cannot bind FOG cofactors. Sonic Hedgehog, an endoderm-derived signaling molecule normally down-regulated in the distal stomach, was over-expressed in hindstomach epithelium of E11.5 Gata4 ki/ki mice, and there was a concomitant decrease in fibroblast growth factor-10 in adjacent mesenchyme. We conclude that functional interaction between GATA-4 and a member of the FOG family, presumably FOG-1, is required for proper epithelial-mesenchymal signaling in the developing stomach. Developmental Dynamics 234:355-362, 2005.

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Section: Discussionmentioning

confidence: 99%

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

Jacobsen¹,

Mannisto²,

Porter-Tinge³

et al. 2005

Developmental Dynamics

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“…Disruption of this transcriptional network results in a variety of human diseases including congenital heart disease, dilated cardiomyopathy, and cardiac hypertrophy (Frey and Olson, 2003;Olson, 2004;Clark et al, 2006). Central to the regulation of these developmental processes are the cardiac transcription factors GATA4 (Watt et al, 2004), NKX2.5 (Cripps and Olson, 2002), Hand (McFadden et al, 2005), nuclear factors of activated T-cell (NFAT) c3 and c4 (Molkentin, 2000;Graef et al, 2001;Bushdid et al, 2003), Foxp4 and FOG2 (Svensson et al, 2000;Lin et al, 2004), and T-box transcription factors TBX1 and TBX5 (Plageman and Yutzey, 2005), all of which have been shown to regulate cardiomyocyte proliferation, cardiacspecific gene expression, and proper patterning of the developing heart.…”

Section: Introductionmentioning

confidence: 99%

Myocardium defects and ventricular hypoplasia in mice homozygous null for the Forkhead Box m1 transcription factor

Ramakrishna

Kim

Petrovič

et al. 2007

Developmental Dynamics

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The Forkhead Box m1 (Foxm1) transcription factor is expressed in cardiomyocytes and cardiac endothelial cells during heart development. In this study, we used a novel Foxm1 ؊/؊ mouse line to demonstrate that Foxm1-deletion causes ventricular hypoplasia and diminished DNA replication and mitosis in developing cardiomyocytes. Proliferation defects in Foxm1 ؊/؊ hearts were associated with a reduced expression of Cdk1-activator Cdc25B phosphatase and NFATc3 transcription factor, and with abnormal nuclear accumulation of the Cdk-inhibitor p21 Cip1 protein. Depletion of Foxm1 levels by siRNA caused altered expression of these genes in cultured HL-1 cardiomyocytes. Endothelial-specific deletion of the Foxm1 fl/fl allele in Tie2-Cre Foxm1 fl/fl embryos did not influence heart development and cardiomyocyte proliferation. Foxm1 protein binds to the ؊9,259/؊9,288-bp region of the endogenous mouse NFATc3 promoter, indicating that Foxm1 is a transcriptional activator of the NFATc3 gene. Foxm1 regulates expression of genes essential for the proliferation of cardiomyocytes during heart development.

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“…Both FOG-1 and FOG-2 have been shown to interact with CtBP-2, but the functional significance of this interaction is unclear, as disruption or deletion of this site in vitro or in vivo does not affect FOG function [9,16,21]. We have previously identified a second domain of FOG proteins localized at the N-terminus of all vertebrate FOG proteins, the FOG repression motif, which is necessary for transcriptional repression [22]. Mutations within this motif abrogate the ability of FOG-1 or FOG-2 to repress GATA-mediated transactivation of target promoters.…”

Section: Introductionmentioning

confidence: 99%

An alternative transcript of the FOG-2 gene encodes a FOG-2 isoform lacking the FOG repression motif

Dale

Remo

Svensson

2007

Biochemical and Biophysical Research Communications

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The FOG family of transcriptional co-factors is composed of two members in mammals: FOG-1 and FOG-2. Both have been shown to bind to GATA factors and function as transcriptional co-repressors in specific cell and promoter contexts. We have previously defined a novel repression domain localized to the N-terminus of each FOG family member, the FOG Repression Motif, which is necessary for FOG-mediated transcriptional repression. In this report, we describe the identification and characterization of a novel isoform of FOG-2 lacking the FOG Repression Motif. In contrast to full-length FOG-2, this isoform is expressed predominately in the embryonic and adult heart. It can bind GATA4 avidly, but is unable to repress GATA4-mediated activation of cardiac-restricted gene promoters. Together, these results suggest that FOG-2 repressive activity may be modulated by the generation of isoforms of FOG-2 lacking the FOG repression motif.

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The N Termini of Friend of GATA (FOG) Proteins Define a Novel Transcriptional Repression Motif and a Superfamily of Transcriptional Repressors

Abstract: Members of the

Cited by 63 publications

References 46 publications

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

GATA‐4:FOG interactions regulate gastric epithelial development in the mouse

Myocardium defects and ventricular hypoplasia in mice homozygous null for the Forkhead Box m1 transcription factor

An alternative transcript of the FOG-2 gene encodes a FOG-2 isoform lacking the FOG repression motif

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