Steroid Receptors and Vertebrate Evolution

Mapping Intimacies ◽

10.32942/osf.io/kpdfq ◽

2019 ◽

Author(s):

Michael Baker

Keyword(s):

Estrogen Receptor ◽

Stress Responses ◽

Steroid Receptors ◽

Estrogen Receptor Α ◽

Cambrian Explosion ◽

Mineralocorticoid Receptors ◽

Basal Chordates ◽

Terrestrial Vertebrates ◽

Evolutionary Success ◽

Life On Earth

Considering that life on earth evolved about 3.7 billion years ago, vertebrates are young, appearing in the fossil record during the Cambrian explosion about 542 to 515 million years ago. Results from sequence analyses of genomes from bacteria, yeast, plants, invertebrates and vertebrates indicate that receptors for adrenal steroids (aldosterone, cortisol), and sex steroids (estrogen, progesterone, testosterone) also are young, with an estrogen receptor and a 3-ketosteroid receptor first appearing in basal chordates (cephalochordates: amphioxus), which are close ancestors of vertebrates. Through gene duplication and divergence of the 3-ketosteroid receptor, receptors that respond to androgens, glucocorticoids, mineralocorticoids and progestins evolved in vertebrates. Thus, an ancestral progesterone receptor and an ancestral corticoid receptor, the common ancestor of the glucocorticoid and mineralocorticoid receptors, evolved in jawless vertebrates (cyclostomes: lampreys, hagfish). This was followed by evolution of an androgen receptor, distinct glucocorticoid and mineralocorticoid receptors and estrogen receptor-α and -β in cartilaginous fishes (gnathostomes: sharks). Further evolution of mineralocorticoid signaling occurred with the evolution of aldosterone synthase in lungfish, a forerunner of terrestrial vertebrates. Adrenal and sex steroid receptors are not found in echinoderms: and hemichordates, which are ancestors in the lineage of cephalochordates and vertebrates. The evolution of steroid receptors at key nodes in the evolution of vertebrates, in which steroid receptors act as master switches to regulate differentiation, development, reproduction, immune responses, electrolyte homeostasis and stress responses, argues for an important role for steroid receptors in the evolutionary success of vertebrates, considering that the human genome contains about 22,000 genes, which is not much larger than genomes of invertebrates, such as Caenorhabditis elegans (~18,000 genes) and Drosophila (~14,000 genes).

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Steroid Receptors and Vertebrate Evolution

10.32942/osf.io/xct2w ◽

2019 ◽

Author(s):

Michael Baker

Keyword(s):

Stress Responses ◽

Steroid Receptors ◽

Cambrian Explosion ◽

Mineralocorticoid Receptors ◽

Basal Chordates ◽

Electrolyte Homeostasis ◽

Evolutionary Success ◽

The Common ◽

Life On Earth ◽

Corticoid Receptor

Considering that life on earth evolved about 3.7 billion years ago, vertebrates are young, appearing in the fossil record during the Cambrian explosion about 542 to 515 million years ago. Results from sequence analyses of genomes from bacteria, yeast, plants, invertebrates and vertebrates indicate that receptors for adrenal steroids (aldosterone, cortisol), and sex steroids (estrogen, progesterone, testosterone) also are young, with receptors for estrogens and 3-ketosteroids first appearing in basal chordates (cephalochordates: amphioxus), which are close ancestors of vertebrates. An ancestral progesterone receptor and an ancestral corticoid receptor, the common ancestor of the glucocorticoid and mineralocorticoid receptors, evolved in jawless vertebrates (cyclostomes: lampreys, hagfish). This was followed by evolution of an androgen receptor and distinct glucocorticoid and mineralocorticoid receptors in cartilaginous fishes (gnathostomes: sharks). Adrenal and sex steroid receptors are not found in echinoderms: and hemichordates, which are ancestors in the lineage of cephalochordates and vertebrates. The presence of steroid receptors in vertebrates, in which these steroid receptors act as master switches to regulate differentiation, development, reproduction, immune responses, electrolyte homeostasis and stress responses, argues for an important role for steroid receptors in the evolutionary success of vertebrates, considering that the human genome contains about 22,000 genes, which is not much larger than genomes of invertebrates, such as Caenorhabditis elegans (~18,000 genes) and Drosophila (~14,000 genes).

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Steroid Receptors and Vertebrate Evolution

10.20944/preprints201901.0313.v1 ◽

2019 ◽

Author(s):

Michael Baker

Keyword(s):

Stress Responses ◽

Steroid Receptors ◽

Cambrian Explosion ◽

Mineralocorticoid Receptors ◽

Basal Chordates ◽

Electrolyte Homeostasis ◽

Evolutionary Success ◽

The Common ◽

Life On Earth ◽

Corticoid Receptor

Considering that life on earth evolved about 3.7 billion years ago, vertebrates are young, appearing in the fossil record during the Cambrian explosion about 542 to 515 million years ago.  Results from sequence analyses of genomes from bacteria, yeast, plants, invertebrates and vertebrates indicate that receptors for adrenal steroids (aldosterone, cortisol), and sex steroids (estrogen, progesterone, testosterone) also are young, with receptors for estrogens and 3-ketosteroids first appearing in basal chordates (cephalochordates: amphioxus), which are close ancestors of vertebrates.  An ancestral progesterone receptor and an ancestral corticoid receptor, the common ancestor of the glucocorticoid and mineralocorticoid receptors, evolved in jawless vertebrates (cyclostomes: lampreys, hagfish).  This was followed by evolution of an androgen receptor and distinct glucocorticoid and mineralocorticoid receptors in cartilaginous fishes (gnathostomes: sharks).  Adrenal and sex steroid receptors are not found in echinoderms: and hemichordates, which are ancestors in the lineage of cephalochordates and vertebrates.  The presence of steroid receptors in vertebrates, in which these steroid receptors act as master switches to regulate differentiation, development, reproduction, immune responses, electrolyte homeostasis and stress responses, argues for an important role for steroid receptors in the evolutionary success of vertebrates, considering that the human genome contains about 22,000 genes, which is not much larger than genomes of invertebrates, such as Caenorhabditis elegans (~18,000 genes) and Drosophila (~14,000 genes).

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Steroid receptors in the adult zebra finch syrinx: a sex difference in androgen receptor mRNA, minimal expression of estrogen receptor α and aromatase

General and Comparative Endocrinology ◽

10.1016/j.ygcen.2003.12.017 ◽

2004 ◽

Vol 136 (2) ◽

pp. 192-199 ◽

Cited By ~ 27

Author(s):

Sean L. Veney ◽

Juli Wade

Keyword(s):

Estrogen Receptor ◽

Androgen Receptor ◽

Sex Difference ◽

Zebra Finch ◽

Steroid Receptors ◽

Estrogen Receptor Α ◽

Receptor Mrna

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Acquisition of Sexual Receptivity: Roles of Chromatin Acetylation, Estrogen Receptor-α, and Ovarian Hormones

Endocrinology ◽

10.1210/en.2010-1001 ◽

2011 ◽

Vol 152 (8) ◽

pp. 3172-3181 ◽

Cited By ~ 21

Author(s):

Paul J. Bonthuis ◽

James K. Patteson ◽

Emilie F. Rissman

Keyword(s):

Estrogen Receptor ◽

Sodium Butyrate ◽

Steroid Receptors ◽

Ovarian Hormones ◽

Estrogen Receptor Α ◽

Sexual Receptivity ◽

Sexually Active ◽

Concurrent Treatment ◽

Deacetylase Inhibitor ◽

Chromatin Acetylation

Sexually naïve, hormone-primed, C57BL/6J female mice are not receptive to mating attempts by conspecific males. Repeated experience with sexually active males and concurrent treatment with estradiol and progesterone gradually increases female receptivity over the course of five trials to maximal levels. Ovarian hormones activate their cognate nuclear steroid receptors estrogen receptor-α and progesterone receptor to induce female sexual receptivity. Nuclear receptors recruit coactivators of transcription that include histone acetyltransferases to hormone responsive genes. In this set of studies, we found that the histone deacetylase inhibitor sodium butyrate enhances the experiential acquisition of receptivity. Evidence is provided that the actions of sodium butyrate on receptivity require activated estrogen receptor-α and progesterone.

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Role of aspartate 351 in transactivation and active conformation of estrogen receptor α

Journal of Molecular Endocrinology ◽

10.1677/jme.1.01846 ◽

2005 ◽

Vol 35 (3) ◽

pp. 449-464 ◽

Cited By ~ 6

Author(s):

Jeong Hoon Kim ◽

Mee Hyun Lee ◽

Byoung Jin Kim ◽

Jun Hyun Kim ◽

Seong Jun Han ◽

...

Keyword(s):

Estrogen Receptor ◽

Dna Binding ◽

Transcriptional Activation ◽

Transcriptional Activity ◽

Steroid Receptors ◽

Estrogen Receptor Α ◽

Orphan Nuclear Receptor ◽

Active Conformation ◽

Wild Type

Estrogen-dependent transcriptional activation by estrogen receptor α (ERα) depends on the conformation of helices 3 and 12 in the ligand-binding domain. To better understand the function of helix 3 in ERα, we examined the role of charged residues, which are conserved in most steroid receptors in helix 3, in estrogen-dependent transactivation. The replacement of Asp-351 with lysine (D351K) or leucine (D351 L) completely abolished estrogen-dependent transactivation without affecting estrogen-binding, DNA-binding and homodimerization activities in ERα. The mutations dramatically reduced the ligand-dependent activation function 2 activity and impaired the ability of ERα to bind p160 coactivators. In addition, the D351K mutant effectively inhibited the transcriptional activation activity of wild-type ERα. Furthermore Asp-351 was required not only for the estrogen-dependent conformational change of wild-type ERα but also for the constitutive transcriptional activity and ligand-independent active conformation of ERα mutant Y537N. Similarly, in the orphan nuclear receptor called estrogen-related receptor 3 (ERR3), the replacement of Asp-273 (the corresponding amino acid to Asp-351 in ERα) with lysine abolished constitutive transcriptional activity of ERR3 without affecting DNA-binding activity and impaired the ability of the receptor to interact with p160 coactivators. These data suggest a role of Asp-351 in inducing and stabilizing the active conformation of ERα, and our results experimentally confirm the concept that Asp-351 in helix 3 interacts with the amide hydrogen of L540 in helix 12 to form a transcriptionally competent surface for binding p160 coactivators.

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Neonatal Exposure to Bisphenol A Alters Rat Uterine Implantation-Associated Gene Expression and Reduces the Number of Implantation Sites

Endocrinology ◽

10.1210/en.2009-1037 ◽

2011 ◽

Vol 152 (3) ◽

pp. 1101-1111 ◽

Cited By ~ 80

Author(s):

Jorgelina Varayoud ◽

Jorge G. Ramos ◽

Verónica L. Bosquiazzo ◽

Melina Lower ◽

Mónica Muñoz-de-Toro ◽

...

Keyword(s):

Gene Expression ◽

Estrogen Receptor ◽

Bisphenol A ◽

Steroid Receptors ◽

Estrogen Receptor Α ◽

Receptor Expression ◽

Female Rats ◽

Postnatal Exposure ◽

Long Term Effects ◽

Implantation Sites

Endocrine disrupters have been associated with reproductive pathologies such as infertility and gynecological tumors. Using a rat model of early postnatal exposure to bisphenol A (BPA), we evaluated the long-term effects on 1) female reproductive performance, 2) uterine homeobox A10 (Hoxa10) and Hoxa10-target gene expression, and 3) ovarian steroid levels and uterine estrogen receptor α and progesterone (P) receptor expression. Newborn female rats received vehicle, BPA.05 (0.05 mg/kg · d), BPA20 (20 mg/kg · d), diethylstilbestrol.2 (0.2 μg/kg · d), or diethylstilbestrol 20 (20 μg/kg · d) on postnatal d 1, 3, 5, and 7. A significant decrease in the number of implantation sites was assessed in the xenoestrogen-exposed females. To address the molecular effects of postnatal xenoestrogen exposure on the pregnant uterus, we evaluated the expression of implantation-associated genes on d 5 of pregnancy (preimplantation uterus). All xenoestrogen-treated rats showed a lower expression of Hoxa10. In the same animals, two Hoxa10-downstream genes were misregulated in the uterus. β3Integrin, which is up-regulated by Hoxa10 in controls, was decreased, whereas empty spiracles homolog 2, which is down-regulated by Hoxa10, was increased. Furthermore a clear down-regulation of estrogen receptor α and P receptor expression was detected without changes in estradiol and P serum levels. The early exposure to BPA produced a lower number of implantation sites in association with a defective uterine environment during the preimplantation period. Alterations in the endocrine-regulated Hoxa10 gene pathways (steroid receptors—Hoxa10—β3integrin/empty spiracles homolog 2) could explain, at least in part, the BPA effects on the implantation process.

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