scholarly journals Estrogen Induces Selective Transcription of Caveolin1 Variants in Human Breast Cancer through Estrogen Responsive Element-Dependent Mechanisms

2020 ◽  
Vol 21 (17) ◽  
pp. 5989
Author(s):  
Antonella Romano ◽  
Antonia Feola ◽  
Antonio Porcellini ◽  
Vincenzo Gigantino ◽  
Maurizio Di Bonito ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcriptional Activation ◽  
Protein Isoforms ◽  
Regulatory Control ◽  
Physiological Processes ◽  
Regulatory Circuit ◽  
Estrogen Responsive Element ◽  
Histone H3 Methylation ◽  
Responsive Element ◽  
H3 Acetylation

The estrogen receptor (ER) signaling regulates numerous physiological processes mainly through activation of gene transcription (genomic pathways). Caveolin1 (CAV1) is a membrane-resident protein that behaves as platform to enable different signaling molecules and receptors for membrane-initiated pathways. CAV1 directly interacts with ERs and allows their localization on membrane with consequent activation of ER-non-genomic pathways. Loss of CAV1 function is a common feature of different types of cancers, including breast cancer. Two protein isoforms, CAV1α and CAV1β, derived from two alternative translation initiation sites, are commonly described for this gene. However, the exact transcriptional regulation underlying CAV1 expression pattern is poorly elucidated. In this study, we dissect the molecular mechanism involved in selective expression of CAV1β isoform, induced by estrogens and downregulated in breast cancer. Luciferase assays and Chromatin immunoprecipitation demonstrate that transcriptional activation is triggered by estrogen-responsive elements embedded in CAV1 intragenic regions and DNA-binding of estrogen-ER complexes. This regulatory control is dynamically established by local chromatin changes, as proved by the occurrence of histone H3 methylation/demethylation events and association of modifier proteins as well as modification of H3 acetylation status. Thus, we demonstrate for the first time, an estrogen-ERs-dependent regulatory circuit sustaining selective CAV1β expression.

scholarly journals Neuropeptide B mediates female sexual receptivity in medaka fish, acting in a female-specific but reversible manner

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Towako Hiraki-Kajiyama ◽  
Junpei Yamashita ◽  
Keiko Yokoyama ◽  
Yukiko Kikuchi ◽  
Mikoto Nakajo ◽  
...  
Keyword(s):  
Mating Behavior ◽  
Transcriptional Activation ◽  
Sex Steroid ◽  
Critical Element ◽  
Specific Expression ◽  
Behavioral Studies ◽  
Estrogen Responsive Element ◽  
Mating Behaviors ◽  
Responsive Element ◽  
Female Specific

Male and female animals display innate sex-specific mating behaviors. In teleost fish, altering the adult sex steroid milieu can effectively reverse sex-typical mating behaviors, suggesting remarkable sexual lability of their brains as adults. In the teleost medaka, neuropeptide B (NPB) is expressed female-specifically in the brain nuclei implicated in mating behavior. Here, we demonstrate that NPB is a direct mediator of estrogen action on female mating behavior, acting in a female-specific but reversible manner. Analysis of regulatory mechanisms revealed that the female-specific expression of NPB is dependent on direct transcriptional activation by estrogen via an estrogen-responsive element and is reversed in response to changes in the adult sex steroid milieu. Behavioral studies of NPB knockouts revealed that female-specific NBP mediates female receptivity to male courtship. The female-specific NPB signaling identified herein is presumably a critical element of the neural circuitry underlying sexual dimorphism and lability of mating behaviors in teleosts.

scholarly journals Neuropeptide B mediates female sexual receptivity in medaka fish, acting in a female-specific but reversible manner

2019 ◽  
Author(s):  
Towako Hiraki-Kajiyama ◽  
Junpei Yamashita ◽  
Keiko Yokoyama ◽  
Kohei Hosono ◽  
Yukika Kawabata-Sakata ◽  
...  
Keyword(s):  
Mating Behavior ◽  
Transcriptional Activation ◽  
Sex Steroid ◽  
Critical Element ◽  
Specific Expression ◽  
Behavioral Studies ◽  
Estrogen Responsive Element ◽  
Mating Behaviors ◽  
Responsive Element ◽  
Female Specific

AbstractMale and female animals display innate sex-specific mating behaviors. Among vertebrates, teleosts are unique in that altering the adult sex steroid milieu can reverse sex-typical mating behaviors, suggesting sexual lability of their brains. In the teleost medaka, neuropeptide B (NPB) is expressed female-specifically in the brain nuclei implicated in mating behavior. Here, we demonstrate that NPB is a direct mediator of estrogen action on female mating behavior, acting in a female-specific but reversible manner. Analysis of regulatory mechanisms revealed that the female-specific expression of NPB is dependent on direct transcriptional activation by estrogen via an estrogen-responsive element and is reversed in response to changes in the adult sex steroid milieu. Behavioral studies of NPB knockouts revealed that female-specific NBP mediates female receptivity to male courtship. The female-specific NPB signaling identified herein is presumably a critical element of the neural circuitry underlying sexual dimorphism and lability of mating behaviors in teleosts.

scholarly journals Comprehensive characterization of the complex lola locus reveals a novel role in the octopaminergic pathway via Tyramine beta-hydroxylase activation

2017 ◽  
Author(s):  
Nadja Dinges ◽  
Violeta Morin ◽  
Nastasja Kreim ◽  
Tony D. Southall ◽  
Jean-Yves Roignant
Keyword(s):  
Transcriptional Activation ◽  
Critical Role ◽  
Protein Isoforms ◽  
Regulatory Control ◽  
Loss Of Function ◽  
Transcriptional Regulatory ◽  
Key Enzyme ◽  
Comprehensive Characterization

Summarylongitudinals lacking (lola) is among the most complex genes in Drosophila melanogaster, encoding up to twenty protein isoforms and acting as a key transcription factor in axonal pathfinding and neural reprogramming. Most of previous studies employed loss-of-function alleles disrupting common exons of lola, making it difficult to delineate its functions. To address this issue we have generated specific mutations in each isoform using the CRISPR/Cas9 system. Our targeted screen allows us to revisit the previously demonstrated roles for few isoforms and to demonstrate a specific function for one variant in axon guidance via activation of the microtubule-associated factor Futsch. Importantly, we also reveal a critical role for a second variant in preventing neurodegeneration via the control of the octopaminergic pathway. This variant is expressed almost exclusively in the octopaminergic cells and is involved in the transcriptional activation of a key enzyme of the pathway. Thus, our comprehensive study greatly expands the functional repertoire of Lola functions, and adds novel insights into the transcriptional regulatory control of neurotransmitter expression in vivo.

Efp as a primary estrogen‐responsive gene in human breast cancer.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Promoter Activity ◽  
Breast Tumors ◽  
Human Breast ◽  
Estrogen Responsive Element ◽  
Estrogen Responsive Gene ◽  
Responsive Gene ◽  
Responsive Element

We have previously isolated the efp (estrogenresponsivefinger protein) that is required for the normalestrogen-induced cell proliferation. Here, we show the genomicorganization of the human efp gene which consists of nine exons.The efp mRNA was expressed in human breast tumors and theestrogen-induced expression of the efp was found in MCF-7human breast cancer cells. Moreover, efp promoter activity wasenhanced through the estrogen-responsive element dependent onestrogen and estrogen receptor. These results suggest that the efpcan mediate estrogen actions such as cell growth in human breastcancer as a primary responsive gene.

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