An Analysis of Retinoic Acid-induced Gene Expression and Metabolism in AB1 Embryonic Stem Cells

Chen, Anne C.; Gudas, Lorraine J.

doi:10.1074/jbc.271.25.14971

Cited by 52 publications

(53 citation statements)

References 85 publications

(46 reference statements)

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“…All genotypes were verified by Southern blotting. WT, RARE-KO, and RAR␥-KO ESCs were cultured as described previously (78). All experiments were performed in the presence of leukemia inhibitory factor (Millipore, Billerica, MA).…”

Section: Methodsmentioning

confidence: 99%

Epigenomic Reorganization of the Clustered Hox Genes in Embryonic Stem Cells Induced by Retinoic Acid

Kashyap¹,

Gudas

Brenet

et al. 2011

Journal of Biological Chemistry

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113

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Section: Methodsmentioning

confidence: 99%

Epigenomic Reorganization of the Clustered Hox Genes in Embryonic Stem Cells Induced by Retinoic Acid

Kashyap¹,

Gudas

Brenet

et al. 2011

Journal of Biological Chemistry

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113

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“…They are derived from the inner cell mass of blastocysts and provide a powerful model system to study the molecular mechanisms regulating early and late lineage specific differentiation. Differentiation of mouse ES (mES) cells can be induced by withdrawal of leukemia inhibitory factor (LIF) from plated cells, the formation of embryoid bodies (EBs) derived by growth of non-adherent mES cells in the absence of LIF, or by treatment of either plated cells or EBs with retinoic acid (RA) [6][7][8][9][10][11][12][13]. In addition, thyroid hormone treatment can modulate the differentiation process in these cells [14,15].…”

Section: Introductionmentioning

confidence: 99%

Differentiation of murine embryonic stem cells induces progesterone receptor gene expression

Sauter

McDermid

Weinberg

et al. 2005

Experimental Cell Research

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The role of steroid hormone receptors in very early embryonic development remains unknown. Clearly, expression during organogenesis is important for tissue-specific development. However, progesterone receptor (PR) and estrogen receptors (ERα, ERβ), are expressed during early development through the blastocyst stage in mice and other species, and yet are not essential for embryonic viability. We have utilized the mouse embryonic stem (mES) cell model to investigate the regulated expression of these receptors during differentiation. Surprisingly, one of the earliest changes in gene expression in response to a differentiation signal observed is PR gene induction. It parallels the time course of expression for the patterning genes Hoxb1 and Hoxa5. Unexpectedly, PR gene expression is not regulated in an estrogen dependent manner by endogenous ERs or by transiently overexpressed ERα. Our results suggest a potentially novel mechanism of PR gene regulation within mES cells compared to adult tissues and the possibility of unique targets of PR action during early mES cell differentiation

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“…We examined the effect of RA treatment on the expression of Nnat mRNA in the three Hoxa1 ES cell lines to validate the microarray results. For comparison purposes, the effect of RA was also examined in the well established AB1 murine embryonic stem cell line (34) (Fig. 5A, lanes 1-7).…”

Section: Expression Of Polycomb Group Genes In the Emc-eshoxa1-15mentioning

confidence: 99%

“…Northern Blot Assays-Total RNA samples were isolated from cells and then subjected to Northern blot analysis as described previously (34). RNA was fractionated by size on 1% agarose, 2.2 M formaldehyde gels, transferred to nylon filters, and cross-linked using a UV Stratalinker 1800.…”

Section: Karyotyping Of Emc-es-hoxa1mentioning

confidence: 99%

Differences in Gene Expression between Wild Type and Hoxa1 Knockout Embryonic Stem Cells after Retinoic Acid Treatment or Leukemia Inhibitory Factor (LIF) Removal

Martinez‐Ceballos

Chambon

Gudas

2005

Journal of Biological Chemistry

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Homeobox (Hox) genes encode a family of transcription factors that regulate embryonic patterning and organogenesis. In embryos, alterations of the normal pattern of Hox gene expression result in homeotic transformations and malformations. Disruption of the Hoxa1 gene, the most 3 member of the Hoxa cluster and a retinoic acid (RA) direct target gene, results in abnormal ossification of the skull, hindbrain, and inner ear deficiencies, and neonatal death. We have generated Hoxa1 genes positioned at the 3Ј-end are expressed earlier and more anterior, whereas 5Ј-end genes are expressed at later times and more posterior (reviewed in Refs. 1 and 5). Colinear gene expression from these Hox gene clusters may involve an initial change in chromatin structure (histone modification and chromatin decondensation) of the entire loci, which would then facilitate the programmed expression of genes along the clusters by a progressive 3Ј to 5Ј change in higher order chromatin structure (6). Treatment of teratocarcinoma cells or embryonic stem cells with retinoic acid (RA), which acts via the retinoic acid receptors (RAR␣, -␤, and -␥ and their isoforms (reviewed in Refs. 7 and 8), results in the sequential activation of several Hox genes in a manner that resembles their positions in the clusters, e.g. 3Ј genes are activated before 5Ј genes (7-9). Moreover, our laboratory discovered the presence of a retinoic acid response element (RARE) in the 3Ј enhancer of the Hoxa1 gene (10 -13). This RARE is also functional in transgenic mice (14 -16). We also demonstrated that unlike F9 Wt cells, F9 RAR␥ Ϫ/Ϫ cells fail to express the Hoxa1 gene in response to RA (17). Alterations in the normal pattern of Hox gene expression in embryos result in homeotic transformations and malformations, and frequently, in perinatal lethality (3,18). For instance, the targeted inactivation in mice of both alleles of the most 3Ј member of the Hoxa cluster, the Hoxa1 gene, leads to numerous developmental defects, including hindbrain deficiencies and abnormal skull ossification, and ultimately, to neonatal death (19 -22). Numerous studies have demonstrated that the hindbrain defects in Hoxa1 Ϫ/Ϫ mice result in part from the failure of Hoxb1 to reach its anterior limit of expression at the presumptive rhombomere 3/rhombomere 4 (r3/4) boundary, which initiates a cascade of gene misexpression that results in the misspecification of the hindbrain compartments from r2 to r5 (23-26). Furthermore, the ectopic expression of Hoxa1 in transgenic mice leads to the ectopic activation of Hoxb1 in r2, produces anterior abnormalities, including the reorganization of the developing hindbrain, and ultimately results in embryonic death (27). These observations highlight the importance of the Hoxa1 gene and suggest that the regulatory effects of retinoids on cell growth and on embryonic patterning may be * This work was supported by National Institutes of Health Grants R01CA43796 (to L. J. G.) and UR 2U19HDO35466. The costs of publication of this article were defrayed in part by th...

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An Analysis of Retinoic Acid-induced Gene Expression and Metabolism in AB1 Embryonic Stem Cells

Cited by 52 publications

References 85 publications

Epigenomic Reorganization of the Clustered Hox Genes in Embryonic Stem Cells Induced by Retinoic Acid

Epigenomic Reorganization of the Clustered Hox Genes in Embryonic Stem Cells Induced by Retinoic Acid

Differentiation of murine embryonic stem cells induces progesterone receptor gene expression

Differences in Gene Expression between Wild Type and Hoxa1 Knockout Embryonic Stem Cells after Retinoic Acid Treatment or Leukemia Inhibitory Factor (LIF) Removal

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