Immunolocalization of estrogen receptor protein in the mouse blastocyst during normal and delayed implantation.

Hou, Qunfang; Paria, Bibhash C.; Mui, Cecily; Dey, Sudhansu K.; Gorski, Jack

doi:10.1073/pnas.93.6.2376

Cited by 62 publications

(24 citation statements)

References 22 publications

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“…In the developing mouse embryo, ERα, ERβ, and PR are expressed at the blastocyst stage and thereafter [16][17][18][19][20][21][22][23]. The expression of these receptors in mES cells may not directly reflect the same timing as in development, but their expression in mES cells allows us to use it as a model system of in vitro differentiation.…”

Section: Discussionmentioning

confidence: 99%

“…Other members of the nuclear receptor family, estrogen receptor alpha (ERα), estrogen receptor beta (ERβ), and progesterone receptor (PR) are present in the early developing embryo of mice and other species [16][17][18][19][20][21][22][23]. In particular, ERα is present in the oocyte, shows variable expression through the morula stage, followed by increased expression in the inner cell mass of the blastocyst.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…Last, during mouse embryonic development, ER has been reported to preferentially accumulate within the nucleolar region of a specific subset of cells (Hou et al, 1996). Because this recompartmentalization is observed during the ontogeny of ERϪ from ERϩ cells, it has been suggested that this recompartmentalization might be a consequence of the mechanism involved in ER downregulation.…”

Section: Visualization Of Human Estrogen Receptormentioning

confidence: 99%

Direct Visualization of the Human Estrogen Receptor α Reveals a Role for Ligand in the Nuclear Distribution of the Receptor

Htun

Holth

Walker

et al. 1999

MBoC

241

148

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The human estrogen receptor ␣ (ER ␣) has been tagged at its amino terminus with the S65T variant of the green fluorescent protein (GFP), allowing subcellular trafficking and localization to be observed in living cells by fluorescence microscopy. The tagged receptor, GFP-ER, is functional as a ligand-dependent transcription factor, responds to both agonist and antagonist ligands, and can associate with the nuclear matrix. Its cellular localization was analyzed in four human breast cancer epithelial cell lines, two ERϩ (MCF7 and T47D) and two ERϪ (MDA-MB-231 and MDA-MB-435A), under a variety of ligand conditions. In all cell lines, GFP-ER is observed only in the nucleus in the absence of ligand. Upon the addition of agonist or antagonist ligand, a dramatic redistribution of GFP-ER from a reticular to punctate pattern occurs within the nucleus. In addition, the full antagonist ICI 182780 alters the nucleocytoplasmic compartmentalization of the receptor and causes partial accumulation in the cytoplasm in a process requiring continued protein synthesis. GFP-ER localization varies between cells, despite being cultured and treated in a similar manner. Analysis of the nuclear fluorescence intensity for variation in its frequency distribution helped establish localization patterns characteristic of cell line and ligand. During the course of this study, localization of GFP-ER to the nucleolar region is observed for ERϪ but not ERϩ human breast cancer epithelial cell lines. Finally, our work provides a visual description of the "unoccupied" and ligand-bound receptor and is discussed in the context of the role of ligand in modulating receptor activity. INTRODUCTIONSteroid hormones elicit diverse biological responses, important during growth, differentiation, inflammation, pregnancy, and homeostasis among many other processes. The genomic actions of steroid hormones are mediated by steroid receptors, members of the nuclear receptor superfamily of ligand-dependent transcription factors. In the absence of hormone, steroid receptors exist in a complex with chaperone proteins capable of high-affinity binding to steroid hormones. Hormone binding leads to a conformational change in the receptor that results in its dissociation from chaperone proteins and ultimately in the binding of the receptor as a homodimer to cognate sites in steroid-responsive genes (reviewed in Tsai and O'Malley, 1994;Mangelsdorf et al., 1995;Beato et al., 1996).Immunohistochemistry and biochemical fractionation show the unoccupied steroid receptors to reside ‡ These authors contributed equally to this work. Corresponding author. E-mail address: hagerg@exchange.nih.gov. predominantly in the cytoplasm, the nucleus, or both compartments, depending on the receptor, in a complex with chaperone proteins (Jensen, 1991;DeFranco et al., 1995;Beato et al., 1996;Pratt and Toft, 1997). For the predominantly nuclear receptors, such as the estrogen receptor (ER), the unoccupied receptor exists in the nucleus either bound or not bound to its cognate site in target genes. ...

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“…However, exogenous oestrogen can cause gonadal sex reversal and ovarian development in a male marsupial young if administered before gonadal differentiation (Burns 1956, 1961, Coveney et al 2001, suggesting that SRY offers the foetus no such protection. Furthermore, ERs are expressed in the foetal gonads of mice and humans despite their apparent redundancy at this time, thereby providing a mechanism through which oestrogen could exert its effects if it were present (Greco et al 1992, Hou & Gorski 1993, Hou et al 1996.…”

Section: Introductionmentioning

confidence: 99%

Ontogeny of the oestrogen receptors ESR1 and ESR2 during gonadal development in the tammar wallaby, Macropus eugenii

Calatayud¹,

Pask²,

Shaw³

et al. 2010

Reproduction

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Oestrogen has wide ranging effects in development mediated mainly via the two oestrogen receptors, a (ESR1, also known as ERa) and b (ESR2, also known as ERb). Oestrogen is the key factor that directs the indifferent gonad to become an ovary in many non-mammalian vertebrates. Oestrogen is not required for early ovarian differentiation in mammals but can disrupt normal testicular development in eutherians. Surprisingly, exogenous oestrogen can cause sex reversal of an XY gonad in two marsupials, the North American opossum and the tammar wallaby. To understand the mechanism by which oestrogen induces sex reversal, we characterised the genes for ESR1 and ESR2 and examined their expression during gonadal differentiation in the tammar wallaby, Macropus eugenii. Both receptors were expressed in the somatic cells and germ cells of the indifferent gonad in both XX and XY foetuses throughout all stages of development, and persisted in these cells into adulthood. ERs were also present in many other tissues including kidney, pituitary and mammary gland. ER mRNA was not significantly altered by exogenous oestrogen in cultured XY gonads but the receptors translocated to the nucleus in its presence. These findings confirm that there is conserved expression of the ERs in the indifferent gonad despite the lack of available ligand during early gonadal development. The receptors can respond to exogenous estrogen at this early stage and are capable of transducing signals in the early mammalian gonad. However, the selective forces that maintained conserved ER expression in this tissue remain unknown.

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Immunolocalization of estrogen receptor protein in the mouse blastocyst during normal and delayed implantation.

Cited by 62 publications

References 22 publications

Differentiation of murine embryonic stem cells induces progesterone receptor gene expression

Differentiation of murine embryonic stem cells induces progesterone receptor gene expression

Direct Visualization of the Human Estrogen Receptor α Reveals a Role for Ligand in the Nuclear Distribution of the Receptor

Ontogeny of the oestrogen receptors ESR1 and ESR2 during gonadal development in the tammar wallaby, Macropus eugenii

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