Transcriptional regulation of the murine k-FGF gene in embryonic cell lines

Gao, Yan; Rosfjord, Edward; Huebert, Claire; Wilder, Phillip J.; Tiesman, Jay P.; Kelly, David L.; Rizzino, Angie

doi:10.1016/0012-1606(92)90046-j

Cited by 65 publications

(108 citation statements)

References 32 publications

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“…The Fgf-4 gene is an octamer-containing enhancer in its 3 0 noncoding region and has been demonstrated to respond to Oct-4 gene (Yuan et al 1996, Ambrosetti et al 1997, Daniels et al 2000. Studies in mouse have shown that this gene is coexpressed with Oct-4 in the ICM and epiblast (Ma et al 1992, Niswander & Martin 1992. Recently, the effect of down-regulation of Oct-4 transcript using dsRNA on the expression of other genes in mouse embryos has been investigated using annealing control primer technique (Shin et al 2005) whereby, of the ten genes, eight (Atp6ap2, GK003, Ddb1, hRscp, Dppa1, Dpp3, Sap18, and Rent1) were down-regulated and two (Rps14 and ETIF2B) were up-regulated in Oct-4 dsRNAinjected blastocysts.…”

Section: Discussionmentioning

confidence: 99%

Selective degradation of maternal and embryonic transcripts in in vitro produced bovine oocytes and embryos using sequence specific double-stranded RNA

Nganvongpanit

Müller²,

Rings³

et al. 2006

Reproduction

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RNA interference (RNAi) has been used for selective degradation of an mRNA transcript or inhibiting its translation to a functional protein in various species. Here, we applied the RNAi approach to suppress the expression of the maternal transcript C-mos and embryonic transcripts Oct-4 in bovine oocytes and embryos respectively, using microinjection of sequence-specific double-stranded RNA (dsRNA). For this, 435 bp C-mos and 341 bp Oct-4 dsRNA were synthesized and microinjected into the cytoplasm of immature oocytes and zygotes respectively. In experiment 1, immature oocytes were categorized into three groups: those injected with C-mos dsRNA, RNase-free water and uninjected controls. In experiment 2, in vitro produced zygotes were categorized into three groups: those injected with Oct-4 dsRNA, RNase-free water and uninjected controls. The developmental phenotypes, the level of mRNA and protein expression were investigated after treatment in both experiments. Microinjection of C-mos dsRNA has resulted in 70% reduction of C-mos transcript after maturation compared to the water-injected and uninjected controls (P!0.01). Microinjection of zygotes with Oct-4 dsRNA has resulted in 72% reduction in transcript abundance at the blastocyst stage compared to the uninjected control zygotes (P!0.01). Moreover, a significant reduction in the number of inner cell mass (ICM) cells was observed in Oct-4 dsRNA-injected embryos compared to the other groups. From oocytes injected with C-mos dsRNA, 60% showed the extrusion of the first polar body compared to 50% in water-injected and 44% in uninjected controls. Moreover, only oocytes injected with C-mos dsRNA showed spontaneous activation. In conclusion, our results demonstrated that sequence-specific dsRNA can be used to knockdown maternal or embryonic transcripts in bovine embryogenesis.

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Section: Discussionmentioning

confidence: 99%

Selective degradation of maternal and embryonic transcripts in in vitro produced bovine oocytes and embryos using sequence specific double-stranded RNA

Nganvongpanit

Müller²,

Rings³

et al. 2006

Reproduction

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“…Mutations either in the Octa site or in the Rox-1 binding sequences compromise the ability of Oct-3/4 to activate the Rex-1 promoter. Oct-3/4 protein possesses the ability to enhance expression of several additional genes, including the platelet-derived growth factor ␣ receptor (PDGF␣R [25]) and fibroblast growth factor (FGF-4) genes (10,31,54,75). Interestingly, nucleotides juxtaposed to the octamer motif were found to play a key role in positively (10 g) and a ␤-Gal ⌬DB-containing reference plasmid (1 g) in the absence (Ϫ) or presence of 10 g of wild-type Oct-6, N-terminus-deleted Oct-6 (N157 or N229), C-terminus-deleted Oct-6 (N2C52), and DNA-binding-domain-deleted Oct-6 (N229C52).…”

Section: Discussionmentioning

confidence: 99%

Rex-1, a Gene Encoding a Transcription Factor Expressed in the Early Embryo, Is Regulated via Oct-3/4 and Oct-6 Binding to an Octamer Site and a Novel Protein, Rox-1, Binding to an Adjacent Site

Ben-Shushan

Thompson

Gudas

et al. 1998

Molecular and Cellular Biology

225

167

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The Rex-1 (Zfp-42) gene, which encodes an acidic zinc finger protein, is expressed at high levels in embryonic stem (ES) and F9 teratocarcinoma cells. Prior analysis identified an octamer motif in the Rex-1 promoter which is required for promoter activity in undifferentiated F9 cells and is involved in retinoic acid (RA)-associated reduction in expression. We show here that the Oct-3/4 transcription factor, but not Oct-1, can either activate or repress the Rex-1 promoter, depending on the cellular environment. Rex-1 repression is enhanced by E1A. The protein domain required for Oct-3/4 activation was mapped to amino acids 1 to 35, whereas the domain required for Oct-3/4 repression was mapped to amino acids 61 to 126, suggesting that the molecular mechanisms underlying transcriptional activation and repression differ. Like Oct-3/4, Oct-6 can also lower the expression of the Rex-1 promoter via the octamer site, and the amino-terminal portion of Oct-6 mediates this repression. In addition to the octamer motif, a novel positive regulatory element, located immediately 5 of the octamer motif, was identified in the Rex-1 promoter. Mutations in this element greatly reduce Rex-1 promoter activity in F9 cells. High levels of a binding protein(s), designated Rox-1, recognize this novel DNA element in F9 cells, and this binding activity is reduced following RA treatment. Taken together, these results indicate that the Rex-1 promoter is regulated by specific octamer family members in early embryonic cells and that a novel element also contributes to Rex-1 expression.

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“…In contrast to the self-renewing effect of LIF and BMP4, mESC autocrine stimulation by fibroblast growth factor 4 (Fgf4) [62,63], working through the Mek/Erk signalling pathway, is known to induce mESCs to exit self-renewal and initiate differentiation [64,65]. This pro-differentiation effect of Fgf/Mek/Erk signalling can be further inferred through complementary experiments, whereby chemical inhibition or genetic knockout of Fgf/ Mek/Erk signalling cascade components caused impaired mESC differentiation [64][65][66][67][68].…”

Section: Signalling In Mouse Escsmentioning

confidence: 99%

The transcriptional regulation of pluripotency

Yeo

2012

Cell Res

117

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Abbreviations: 2C (2-cell); 2i (two inhibitor); BMP4 (bone morphogenic protein 4); ChIP (chromatin immunoprecipitation); ChIP-seq (chromatin immunoprecipitation and sequencing); ESCs (embryonic stem cells); EpiSCs (Epiblast-derived stem cells); Fgf4 (fibroblast growth factor 4); hESCs (human embryonic stem cells); ICM (inner cell mass); iPSCs (induced pluripotent stem cells); LIF (leukemia inhibitory factor); lincRNA (large intergenic non-coding RNA); mESCs (mouse embryonic stem cells); miRNA (micro RNA); ncRNA (non-coding RNA); PcG (Polycomb group proteins); PGCs (primodial germ cells); POU (Pit-Oct-Unc); RNAi (RNA interference); RNA-seq (RNA sequencing); SCF (stem cell factor); siRNA (short interfering RNA); XaXa (double X-chromosome active); XaXi (single X-chromosome inactivated)The defining features of embryonic stem cells (ESCs) are their self-renewing and pluripotent capacities. Indeed, the ability to give rise into all cell types within the organism not only allows ESCs to function as an ideal in vitro tool to study embryonic development, but also offers great therapeutic potential within the field of regenerative medicine. However, it is also this same remarkable developmental plasticity that makes the efficient control of ESC differentiation into the desired cell type very difficult. Therefore, in order to harness ESCs for clinical applications, a detailed understanding of the molecular and cellular mechanisms controlling ESC pluripotency and lineage commitment is necessary. In this respect, through a variety of transcriptomic approaches, ESC pluripotency has been found to be regulated by a system of ESC-associated transcription factors; and the external signalling environment also acts as a key factor in modulating the ESC transcriptome. Here in this review, we summarize our current understanding of the transcriptional regulatory network in ESCs, discuss how the control of various signalling pathways could influence pluripotency, and provide a future outlook of ESC research.

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Transcriptional regulation of the murine k-FGF gene in embryonic cell lines

Cited by 65 publications

References 32 publications

Selective degradation of maternal and embryonic transcripts in in vitro produced bovine oocytes and embryos using sequence specific double-stranded RNA

Selective degradation of maternal and embryonic transcripts in in vitro produced bovine oocytes and embryos using sequence specific double-stranded RNA

Rex-1, a Gene Encoding a Transcription Factor Expressed in the Early Embryo, Is Regulated via Oct-3/4 and Oct-6 Binding to an Octamer Site and a Novel Protein, Rox-1, Binding to an Adjacent Site

The transcriptional regulation of pluripotency

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