Regulation of the <i>Lim‐1</i> gene is mediated through conserved FAST‐1/FoxH1 sites in the first intron

Watanabe, Minoru; Rebbert, Martha L.; Andreazzoli, Massimiliano; Takahashi, Nobuhiro; Toyama, Reiko; Zimmerman, Steven; Whitman, Malcolm; Dawid, Igor B.

doi:10.1002/dvdy.10176

Cited by 31 publications

(33 citation statements)

References 61 publications

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“…The midline defects reflect the inability of the embryo to correctly pattern the APS as seen by failure to activate Gsc, Lim1 and Foxa2. The promoter regions of Gsc and Lim1 have been shown to contain activin response elements occupied by a complex containing Smad4, Smad2 and Foxh1 (Labbé et al, 1998;Watanabe et al, 2002), and failure to activate Gsc and Lim1 expression in the APS domain is thus consistent with a essential role for Smad4 in the regulation of these genes. The definitive endoderm arises from cells within the epiblast that ingress through the APS, displacing the visceral endoderm layer.…”

Section: Smad4 and Formation Of The Anterior Primitive Streakmentioning

confidence: 83%

Differential requirements for Smad4 in TGFβ-dependent patterning of the early mouse embryo

et al. 2004

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Genetic and biochemical data have identified Smad4 as a key intracellular effector of the transforming growth factor β (TGFβ superfamily of secreted ligands. In mouse, Smad4-null embryos do not gastrulate, a phenotype consistent with loss of other TGFβ-related signaling components. Chimeric analysis reveals a primary requirement for Smad4in the extra-embryonic lineages; however, within the embryo proper,characterization of the specific roles of Smad4 during gastrulation and lineage specification remains limited. We have employed a Smad4conditional allele to specifically inactivate the Smad4 gene in the early mouse epiblast. Loss of Smad4 in this tissue results in a profound failure to pattern derivatives of the anterior primitive streak, such as prechordal plate, node, notochord and definitive endoderm. In contrast to these focal defects, many well-characterized TGFβ- and Bmp-regulated processes involved in mesoderm formation and patterning are surprisingly unaffected. Mutant embryos form abundant extra-embryonic mesoderm, including allantois, a rudimentary heart and middle primitive streak derivatives such as somites and lateral plate mesoderm. Thus, loss of Smad4 in the epiblast results not in global developmental abnormalities but instead in restricted patterning defects. These results suggest that Smad4 potentiates a subset of TGFβ-related signals during early embryonic development, but is dispensable for others.

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Section: Smad4 and Formation Of The Anterior Primitive Streakmentioning

confidence: 83%

Differential requirements for Smad4 in TGFβ-dependent patterning of the early mouse embryo

et al. 2004

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“…However, the FOXO binding element within the p130 RB2 gene has been mapped within the first intron (36), and a DBE has been identified at an exonintron boundary of the rat bim promoter (26). Regulation of gene expression though sequences located in the first intron has also been described for other forkhead transcription factors (71).…”

Section: Discussionmentioning

confidence: 99%

Induction of Mxi1-SRα by FOXO3a Contributes to Repression of Myc-Dependent Gene Expression

Delpuech

Griffiths

East³

et al. 2007

Molecular and Cellular Biology

159

145

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Forkhead transcription factors of the O class (FOXOs) belong to a family of transcription factors that are characterized by their conserved DNA binding domain (forkhead box). Daf-16, the FOXO orthologue in Caenorhabditis elegans, has been identified as a target of insulin-like signaling through the Daf-2/AGE-1 pathway and is involved in formation of the Dauer stage (40,53). The FOXO subgroup in mammals consists of four members, FOXO1, FOXO3a, and FOXO4 (previously termed FKHR, FKHRL1, and AFX, respectively) and FOXO6 (7,24,33,62).FOXO transcription factors bind to DNA as monomers through their winged-helix domain at a consensus motif termed DBE (for Daf-16 family member binding element) with the core sequence TTGTTAC (23). A number of FOXO target genes have been identified so far (for review, see reference 28). FOXO target genes are involved in cell cycle arrest, apoptosis, metabolism, differentiation, and the stress response. It has been shown that FOXOs induce G 1 arrest through expression of p27 KIP1 and p130 (36,46,51) and increase the duration of the G 2 phase of the cell cycle by inducing cyclin G 2 (43). In lymphocytes, FOXO activation induces cell death through induction of Bim, Trail, and Fas ligand (9,48,66). Upregulation of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase by FOXOs results in induction of gluconeogenesis (5, 30). The role of FOXO transcription factors in differentiation is less well understood and is cell type dependent. In adipocytes, FOXOs inhibit differentiation most likely through induction of p21, while FOXO activation induces erythroid differentiation through induction of BTG and is required for myoblast differentiation (4, 6, 50). Finally, induction of Mn-superoxide dismutase and catalase by FOXO is involved in detoxification of reactive oxygen species (19,34).Mammalian FOXO transcription factors are regulated through the phosphatidylinositol 3-kinase (PI3-kinase) pathway. In the absence of growth factors, FOXOs are localized to the nucleus and transcriptionally active. Activation of Akt or SGK in response to growth factor stimulation induces phosphorylation of FOXO transcription factors at three highly conserved serine and threonine residues (9, 35). As a result, FOXO transcription factors translocate to the cytoplasm. Phos-* Corresponding author. Mailing address: Gene

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“…Similarly, mouse embryonic stem cells respond to activin and RA by upregulation of IM markers (Kim and Dressler, 2005). Moreover, both zebrafish and Xenopus Lim1 genes contain an activin response element (ARE) in their first intron, which, at least in zebrafish embryos, is required for the expression of this gene (Rebbert and Dawid, 1997;Watanabe et al, 2002). Previous studies suggest a role for BMP signaling in specifying IM cells and the induction of IM genes (James and Schultheiss, 2005;Obara-Ishihara et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Interplay between activin and Hox genes determines the formation of the kidney morphogenetic field

et al. 2009

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The kidney develops in a specific position along the anterior-posterior axis. All vertebrate kidney tissues are derived from the intermediate mesoderm (IM), and early kidney genes such as Lim1 and Pax2 are expressed in amniotes posterior to the sixth somite axial level. IM cells anterior to this level do not express kidney genes owing to changes in their competence to respond to kidneyinductive signals present along the entire axis. We aimed to understand the molecular mechanisms governing the loss of competence of anterior IM cells and the formation of the anterior border of the kidney morphogenetic field. We identified the dorsal neural tube as the potential kidney-inductive tissue and showed that activin, a secreted morphogen, is necessary but insufficient for Lim1 induction and establishment of the kidney field. Activin or activin-like and BMP signaling cascades are activated along the entire axis, including in anterior non-kidney IM, suggesting that competence to respond to these signals involves downstream or other components. Detailed expression pattern analysis of Hox genes during early chick development revealed that paralogous group four genes share the same anterior border as the kidney genes. Ectopic expression of Hoxb4 in anterior non-kidney IM, either by retinoic acid (RA) administration or plasmid-mediated overexpression, resulted in ectopic kidney gene expression. The anterior expansion of Lim1 expression was restrained when Hoxb4 was co-expressed with a truncated form of activin receptor. We suggest a model in which the competence of IM cells to respond to TGFβ signaling and express kidney genes is driven by RA and mediated by Hoxb4.

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Regulation of the Lim‐1 gene is mediated through conserved FAST‐1/FoxH1 sites in the first intron

Abstract: The Lim-1 gene encodes a LIMhomeodomain transcription factor that is highly conserved among vertebrates and is required for successful gastrulation and head formation.

Cited by 31 publications

References 61 publications

Differential requirements for Smad4 in TGFβ-dependent patterning of the early mouse embryo

Differential requirements for Smad4 in TGFβ-dependent patterning of the early mouse embryo

Induction of Mxi1-SRα by FOXO3a Contributes to Repression of Myc-Dependent Gene Expression

Interplay between activin and Hox genes determines the formation of the kidney morphogenetic field

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