Estrogen Receptor Inhibits Mineralocorticoid Receptor Transcriptional Regulatory Function

The transcriptional regulatory function of estrogen receptor β (ESR2) is essential for the regulation of primordial follicle activation (PFA). Increased PFA due to the loss of ESR2 becomes evident as early as postnatal day 8 (PND8). To identify the ESR2-regulated genes that control PFA, we performed RNA-seq analyses of wildtype, and Esr2 knockout (Esr2KO) neonatal rat ovaries collected on PND4, PND6, and PND8. Among the differentially expressed genes in Esr2KO ovaries, indian hedgehog (Ihh) displayed the highest downregulation among the ovary enriched genes. IHH regulated genes including Hhip as well as the steroidogenic enzymes were also downregulated in Esr2KO rat ovaries. Remarkably, the expression of Ihh in Esr2KO ovaries was not upregulated despite the high levels of Gdf9 and Bmp15, which are known regulators of Ihh expression in granulosa cells. Our findings suggest that indian hedgehog signaling in the neonatal rat ovary is dependent on ESR2.

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RPD3 encodes a second factor required to achieve maximum positive and negative transcriptional states in Saccharomyces cerevisiae

Molecular and Cellular Biology ◽

10.1128/mcb.11.12.6317-6327.1991 ◽

1991 ◽

Vol 11 (12) ◽

pp. 6317-6327 ◽

Cited By ~ 1

Author(s):

M Vidal ◽

R F Gaber

Keyword(s):

Saccharomyces Cerevisiae ◽

Target Genes ◽

Current Data ◽

Regulatory Function ◽

Fourfold Increase ◽

Recessive Mutations ◽

Activation Of Transcription ◽

Transcriptional Regulatory ◽

Low Levels ◽

Full Activation

In Saccharomyces cerevisiae, TRK1 and TRK2 encode the high- and low-affinity K+ transporters, respectively. In cells containing a deletion of TRK1, transcription levels of TRK2 are extremely low and are limiting for growth in media containing low levels of K+ (Trk- phenotype). Recessive mutations in RPD1 and RPD3 suppress the TRK2, conferring an approximately fourfold increase in transcription. rpd3 mutations confer pleiotropic phenotypes, including (i) mating defects, (ii) hypersensitivity to cycloheximide, (iii) inability to sporulate as homozygous diploids, and (iv) constitutive derepression of acid phosphatase. RPD3 was cloned and is predicted to encode a 48-kDa protein with no extensive similarity to proteins contained in current data bases. Deletion of RPD3 is not lethal but confers phenotypes identical to those caused by spontaneous mutations. RPD3 is required for both full repression and full activation of transcription of target genes including PHO5, STE6, and TY2. RPD3 is the second gene required for this function, since RPD1 is also required. The effects of mutations in RPD1 and RPD3 are not additive, suggesting that these genes are involved in the same transcriptional regulatory function or pathway.

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The bcl-2 major breakpoint region (mbr) possesses transcriptional regulatory function

Gene ◽

10.1016/j.gene.2006.05.002 ◽

2006 ◽

Vol 379 ◽

pp. 127-131 ◽

Cited By ~ 11

Author(s):

Jingjing Zhang ◽

Changyan Ma ◽

Xiao Han ◽

Linda K. Durrin ◽

Yujie Sun

Keyword(s):

Breakpoint Region ◽

Regulatory Function ◽

Transcriptional Regulatory

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Spindle Assembly Checkpoint Protein Cdc20 Transcriptionally Activates Expression of Ubiquitin Carrier Protein UbcH10

Journal of Biological Chemistry ◽

10.1074/jbc.m110.160671 ◽

2011 ◽

Vol 286 (18) ◽

pp. 15666-15677 ◽

Cited By ~ 12

Author(s):

Somsubhra Nath ◽

Taraswi Banerjee ◽

Debrup Sen ◽

Tania Das ◽

Susanta Roychoudhury

Keyword(s):

Chromosomal Instability ◽

Spindle Assembly Checkpoint ◽

Spindle Assembly ◽

Regulatory Function ◽

Physical Interaction ◽

Anaphase Promoting Complex ◽

Transcriptional Regulatory ◽

Subsequent Degradation ◽

Ubiquitin Conjugating Enzyme ◽

Wd40 Domain

The spindle assembly checkpoint (SAC) ensures accurate segregation of chromosomes by monitoring kinetochore attachment of spindles during mitosis. Proper progression of mitosis depends on orderly ubiquitination and subsequent degradation of various mitotic inhibitors. At the molecular level, upon removal of SAC, Cdc20 activates E3 ubiquitin ligase anaphase-promoting complex/cyclosome that, along with E2 ubiquitin-conjugating enzyme UbcH10, executes this function. Both Cdc20 and UbcH10 are overexpressed in many cancer types and are associated with defective SAC function leading to chromosomal instability. The precise mechanism of correlated overexpression of these two proteins remains elusive. We show that Cdc20 transcriptionally up-regulates UbcH10 expression. The WD40 domain of Cdc20 is required for this activity. Physical interaction between Cdc20 and anaphase-promoting complex/cyclosome-CBP/p300 complex and its subsequent recruitment to the UBCH10 promoter are involved in this transactivation process. This transcriptional regulatory function of Cdc20 was observed to be cell cycle-specific. We hypothesize that this co-regulated overexpression of both proteins contributes to chromosomal instability.

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Effect of Follicle-Stimulating Hormone and Estrogen on the Expression of Betaglycan Messenger Ribonucleic Acid Levels in Cultured Rat Granulosa Cells

Endocrinology ◽

10.1210/en.2004-1665 ◽

2005 ◽

Vol 146 (8) ◽

pp. 3379-3386 ◽

Cited By ~ 16

Author(s):

Yuki Omori ◽

Kazuto Nakamura ◽

Soichi Yamashita ◽

Hiroko Matsuda ◽

Tetsuya Mizutani ◽

...

Keyword(s):

Estrogen Receptor ◽

Protein Kinase ◽

Protein Kinase A ◽

Granulosa Cells ◽

Luciferase Assay ◽

Regulatory Function ◽

Type Ii ◽

Mrna Transcript ◽

Inhibin A ◽

Kinase A

Abstract Betaglycan (TGFβ type III receptor) was recently identified as a coreceptor to enhance the binding of inhibin A to activin type II receptor. This inhibin/betaglycan/activin type II receptor complex prevents activins from binding to their own receptors. The present study was undertaken to identify the expression and the regulation of the betaglycan gene in cultured rat granulosa cells. Northern blot analysis indicated betaglycan mRNA transcript of approximately 6.4 kbp. The treatment of the cells with FSH increased the betaglycan mRNA level, and a concurrent treatment with estradiol brought a significant increase in betaglycan mRNA. The protein kinase A activator, 8-bromoadenosine-cAMP, also increased the expression of its mRNA. Furthermore, betaglycan mRNA was induced additively by estradiol, which was blocked by estrogen receptor antagonists [ICI 182780, (R, R)-cis-diethyltetrahydro-2,8-chrysenediol]. In the luciferase assay, FSH altered the promoter activity of betaglycan. Moreover, when FSH plus estradiol was added to the granulosa cells, a significant increase in the half-life of betaglycan mRNA transcript was seen. In summary, FSH and estradiol increased betaglycan mRNA expression, most possibly through the protein kinase A pathway and the estrogen receptor-β. The increase of betaglycan mRNA was due to an increase in transcription and altered mRNA stability. In ovarian regulatory function, the expression of betaglycan may involve the functional antagonism of inhibin A in activin signal transduction.

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G Protein-Coupled Estrogen Receptor 1 (GPER1) Mediates Aldosterone-Induced Endothelial Inflammation in a Mineralocorticoid Receptor-Independent Manner

International Journal of Endocrinology ◽

10.1155/2021/5575927 ◽

2021 ◽

Vol 2021 ◽

pp. 1-8

Author(s):

Ziwei Tang ◽

Qifu Li ◽

Qingfeng Cheng ◽

Mei Mei ◽

Ying Song ◽

...

Keyword(s):

Endothelial Cells ◽

Estrogen Receptor ◽

Inflammatory Response ◽

G Protein ◽

Mineralocorticoid Receptor ◽

Umbilical Vein ◽

Vascular Inflammation ◽

Independent Manner ◽

G Protein Coupled ◽

Estrogen Receptor 1

Objective. It has been increasingly appreciated that G protein-coupled estrogen receptor 1 (GPER1) mediates both proinflammatory and anti-inflammatory response of estrogen. It is also involved in some rapid vascular effects of aldosterone in a mineralocorticoid receptor (MR) independent manner. However, whether GPER1 mediates aldosterone-induced inflammation response in endothelial cells and its relationship with MR are yet undetermined and therefore require further explanation. Method. Based on the hypothesis that GPER1 plays a role in the aldosterone-related vascular inflammation, the present study utilized a model of human umbilical vein endothelial cells transfected with MR siRNA and induced for inflammatory response with increasing concentration of aldosterone. Results. It was discovered that induction of aldosterone had no effect on the expression of GPER1 but promoted the expression of MR. Suppression of MR did not influence GPER1 expression, and GPER1 was capable of mediating part of aldosterone-induced endothelial inflammatory response. This effect may involve phosphoinositide 3-kinases (PI3K) pathway signaling. Conclusion. These findings not only demonstrated the role of GPER1 in aldosterone-induced vascular inflammation but also suggested an alternative for pharmaceutical treatment of hyperaldosteronism considering the unsatisfying effect on cardiovascular risks with MR antagonists.

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