Analysis of Transcription Factor AP-2 Expression and Function During Mouse Preimplantation Development1

Winger, Quinton A.; Huang, Jian; Auman, Heidi; Lewandoski, Mark; Williams, Trevor

doi:10.1095/biolreprod.106.052407

Cited by 48 publications

(66 citation statements)

References 56 publications

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“…Detailed spatiotemporal expression analysis showed that AP2γ is expressed in the entire epiblast before HH stage 3 and gradually shifts outwards to the putative epidermal ectoderm at HH stage 4, accompanying with comple- mentary cSox2 expansion. Similarly, mouse AP2γ might have expression changes from ICM at E3.5 [47] to nonneural ectoderm at the late gastrulation stage [48]. The dynamic expression pattern of cAP2γ suggests that AP2γ might play multiple roles in ectodermal patterning in different regions of the epiblast.…”

Section: Discussionmentioning

confidence: 99%

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AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

et al. 2012

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Bone morphogenetic protein (BMP) inhibits neural specification and induces epidermal differentiation during ectodermal patterning. However, the mechanism of this process is not well understood. Here we show that AP2γ, a transcription factor activator protein (AP)-2 family member, is upregulated by BMP4 during neural differentiation of pluripotent stem cells. Knockdown of AP2γ facilitates mouse embryonic stem cell (ESC) neural fate determination and impairs epidermal differentiation, whereas AP2γ overexpression inhibits neural conversion and promotes epidermal commitment. In the early chick embryo, AP2γ is expressed in the entire epiblast before HH stage 3 and gradually shifts to the putative epidermal ectoderm during HH stage 4. In the future neural plate AP2γ inhibits excessive neural expansion and it also promotes epidermal development in the surface ectoderm. Moreover, AP2γ knockdown in ESCs and chick embryos partially rescued the neural inhibition and epidermal induction effects of BMP4. Mechanistic studies showed that BMP4 directly regulates AP2γ expression through Smad1 binding to the AP2γ promoter. Taken together, we propose that during the early stages of ectodermal patterning in the chick embryo, AP2γ acts downstream of the BMP pathway to restrict precocious neural expansion in the prospective neural plate and initiates epidermal differentiation in the future epidermal ectoderm.

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Section: Discussionmentioning

confidence: 99%

“…AP2γ is expressed in the inner cell mass (ICM) and trophectoderm of mouse embryo [32,47], and previous studies have focused on its functions in extraembryonic development. However, the functions of AP2γ during development from ICM to neural/epidermal ectoderm are not fully understood.…”

Section: Discussionmentioning

confidence: 99%

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

et al. 2012

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“…The level of transcripts coding for self-renewal regulators such as Klf4, Esrrb, and Tcl1 was reduced, while trophoblast lineage-associated genes such as Cdx2, Tcfap2a, Fgfr2, Plf, and Mmp9 were coordinately up-regulated (Supplemental Fig. S4; Niwa et al 2005;Strumpf et al 2005;Winger et al 2006) . Although the data support the notion that Eset depletion leads to the formation of trophoblast-like cells, it is also likely that cell types of other lineages are formed (Fig.…”

Section: Depletion Of Eset Induces Es Cell Differentiationmentioning

confidence: 99%

“…Tcfap2a, a member of the activating protein 2 (AP-2) transcription factor family, is preferentially expressed in the TE of the blastocyst (Winger et al 2006). Tcfap2c, another member of the AP-2 family, is expressed throughout the preimplantation period and becomes restricted to the extraembryonic lineages at the time of implantation.…”

Section: Genomic Targets Of Eset Identified By Chromatin Immunoprecipmentioning

confidence: 99%

“…Tcfap2c knockout studies revealed that it is essential in the extraembryonic lineages for early post-implantation development (Auman et al 2002). Double knockout of Tcfap2a and Tcfap2c showed a more severe phenotype than individual knockout, indicating that these genes play redundant roles during the peri-implantation stage, presumably by affecting the trophoblast cell lineage (Winger et al 2006). We confirmed that Tcfap2a expression is induced after Eset depletion ( Fig.…”

Section: Genomic Targets Of Eset Identified By Chromatin Immunoprecipmentioning

confidence: 99%

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Eset partners with Oct4 to restrict extraembryonic trophoblast lineage potential in embryonic stem cells

Yuan

Han²,

Guo³

et al. 2009

Genes Dev.

225

243

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The histone H3 Lys 9 (H3K9) methyltransferase Eset is an epigenetic regulator critical for the development of the inner cell mass (ICM). Although ICM-derived embryonic stem (ES) cells are normally unable to contribute to the trophectoderm (TE) in blastocysts, we find that depletion of Eset by shRNAs leads to differentiation with the formation of trophoblast-like cells and induction of trophoblast-associated gene expression. Using chromatin immmunoprecipitation (ChIP) and sequencing (ChIP-seq) analyses, we identified Eset target genes with Esetdependent H3K9 trimethylation. We confirmed that genes that are preferentially expressed in the TE (Tcfap2a and Cdx2) are bound and repressed by Eset. Single-cell PCR analysis shows that the expression of Cdx2 and Tcfap2a is also induced in Eset-depleted morula cells. Importantly, Eset-depleted cells can incorporate into the TE of a blastocyst and, subsequently, placental tissues. Coimmunoprecipitation and ChIP assays further demonstrate that Eset interacts with Oct4, which in turn recruits Eset to silence these trophoblast-associated genes. Our results suggest that Eset restricts the extraembryonic trophoblast lineage potential of pluripotent cells and links an epigenetic regulator to key cell fate decision through a pluripotency factor.[Keywords: Oct4; embryonic stem cells; histone methylation; pluripotency; transcriptional repression; trophoblast] Supplemental material is available at http://www.genesdev.org.

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Genome‐scale study of transcription factor expression in the branching mouse lung

Herriges

Hines

et al. 2012

Developmental Dynamics

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Background Mammalian lung development consists of a series of precisely choreographed events that drive the progression from simple lung buds to the elaborately branched organ that fulfills the vital function of gas exchange. Strict transcriptional control is essential for lung development. Among the large number of transcription factors encoded in the mouse genome, only a small portion of them are known to be expressed and function in the developing lung. Thus a systematic investigation of transcription factors expressed in the lung is warranted. Results To enrich for genes that may be responsible for regional growth and patterning, we performed a screen using RNA in situ hybridization to identify genes that show restricted expression patterns in the embryonic lung. We focused on the pseudoglandular stage during which the lung undergoes branching morphogenesis, a cardinal event of lung development. Using a genome-scale probe set that represents over 90% of the transcription factors encoded in the mouse genome, we identified sixty-two transcription factor genes with localized expression in the epithelium, mesenchyme or both. Many of these genes have not been previously implicated in lung development. Conclusions Our findings provide new starting points for the elucidation of the transcriptional circuitry that controls lung development.

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Analysis of Transcription Factor AP-2 Expression and Function During Mouse Preimplantation Development1

Cited by 48 publications

References 56 publications

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

AP2γ regulates neural and epidermal development downstream of the BMP pathway at early stages of ectodermal patterning

Eset partners with Oct4 to restrict extraembryonic trophoblast lineage potential in embryonic stem cells

Genome‐scale study of transcription factor expression in the branching mouse lung

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