Mus musculus
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ABSTRACT:
PROVIDER: PRJNA397850 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Regulatory Architecture of the LβT2 Gonadotrope Cell Underlying the Response to Gonadotropin-Releasing Hormone
| PRJNA397847 | ENA
Project description:Regulatory Architecture of the LβT2 Gonadotrope Cell Underlying the Response to Gonadotropin-Releasing Hormone [ATAC-Seq]
| PRJNA397652 | ENA
Project description:We used microarrays to detail the global program of gene expression underlying gonadotropin-releasing hormone (GnRH) generation and delamination from the olfactory placode.
2016-09-30 | GSE87486 | GEO
Project description:Abstract: Peptidylarginine deiminases (PADs or PADIs) catalyze the conversion of positively charged arginine to neutral citrulline, which alters target protein structure and function. It is well established that a gonadotropin releasing hormone agonist (GnRHa) stimulates PAD2-catalyzed histone citrullination to epigenetically regulate gonadotropin gene expression in the gonadotrope derived LBT2 cell line. However, PADs are also found in the cytoplasm. Given this, we used mass spectrometry to identify additional non-histone proteins that are citrullinated following GnRHa stimulation and characterize the temporal dynamics of this modification. Our results show that actin and tubulin are rapidly citrullinated, which led us to hypothesize that GnRHa might induce their citrullination to modulate cytoskeletal dynamics and architecture. Data shows that 10 nM GnRHa induces citrullination of beta-actin with maximal levels occurring at 10 minutes. The level of beta-actin citrullination is reduced in the presence of the pan-PAD inhibitor bi-phenyl-benzimidazole-Cl-amidine (BB-ClA), which also prevents GnRHa induced actin reorganization in dispersed mouse gonadotrope cells. GnRHa induces citrullination of beta-tubulin with elevated levels occurring at 30 minutes; similarly to beta-actin, this response is attenuated in the presence of BB-ClA. To examine the functional consequence of beta-tubulin citrullination, we utilized fluorescently tagged end binding protein 1 (EB1-GFP) to track the growing plus end of microtubules (MT) in real time in transfected LBT2 cells. Time-lapse confocal microscopy of EB1-GFP reveals that MT average lifetime increases following 30 minutes of GnRHa treatment, but this increase is attenuated by PAD inhibition. Taken together, our data suggest that GnRHa induced citrullination alters actin reorganization and MT lifetime in gonadotrope cells.
Keywords: gonadotrope, peptidylarginine deiminase, citrullination, cytoskeleton, beta tubulin, beta actin, microtubules
2024-01-31 | MSV000093973 | MassIVE
Project description:Follicle-stimulating hormone (FSH), a dimeric glycoprotein produced by pituitary gonadotrope cells, regulates spermatogenesis in males and ovarian follicle growth in females. Hypothalamic gonadotropin-releasing hormone (GnRH) stimulates FSHβ subunit gene (Fshb) transcription, though the underlying mechanisms are poorly understood. To address this gap in knowledge, we examined changes in pituitary gene expression in GnRH-deficient mice (hpg) treated with a regimen of exogenous GnRH that increases pituitary Fshb but not luteinizing hormone β (Lhb) mRNA levels. Activating transcription factor 3 (Atf3) was among the most upregulated genes. ATF3 can heterodimerize with members of the AP-1 family to regulate gene transcription. Co-expression of ATF3 with JunB stimulated murine Fshb, but not Lhb, promoter-reporter activity in homologous LβT2 cells. ATF3 also synergized with a constitutively active activin type I receptor to increase endogenous Fshb expression in these cells. Nevertheless, FSH production was intact in gonadotrope-specific Atf3 knockout mice (cKO) and control littermates. Ovarian follicle development, ovulation, and litter sizes were also equivalent between genotypes. Testis weights and sperm counts did not differ between cKO and control males. Following gonadectomy, increases in LH secretion were enhanced in cKO animals. Though FSH levels did not differ between genotypes, post-gonadectomy increases in pituitary Fshb and gonadotropin α subunit expression were more pronounced in cKO mice. These data indicate that ATF3 can selectively stimulate Fshb transcription in vitro but is not required for FSH production in vivo.
2023-06-28 | GSE220809 | GEO
Project description:GT1-7 cells were treated with 100 μg/mL HTR1A antagonist WAY-100635 maleate for 6 h and harvested for investigation on the genome-wide enrichments of CBX4 and H2AK119ub by ChIP-seq. This study aimed to investigate the regulatory mechanism on expression of gonadotropin-releasing hormone affected by HTR1A inhibition.
2021-03-12 | E-MTAB-10173 | biostudies-arrayexpress
Project description:Naked mole rats live in eusocial colonies where subordinates help a single dominant female and a few males to breed. We investigated the genome-wide regulatory mechanisms underlying their reproductive division of labor by examining brain and gonad transcriptomes and DNA-methylomes. Subtle expression differences were observed between brains of dominants and subordinates, but differentially expressed genes clustered consistently in a module with similar function for both sexes. Gonadotropin-releasing hormone (GNRH1) was central in this module and linked with stress-response genes such as neuropeptide Y and corticotrophin-releasing hormone. Breeder-subordinate modifications in DNA methylation were substantial in male brains and associated with the GNRH1 module. The GNRH1-regulated estrogen synthesis pathway was completely blocked in subordinate ovaries and sperm-related genes were significantly down-regulated in subordinate testes. Our results indicate that reproductive suppression is based on hormonal- and stress-related control by the dominant female, but with significant differences in molecular mechanisms between males and females.
2017-03-30 | GSE67542 | GEO
Project description:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes the many forms of reproductive toxicity, such as defects in sexual behaviors, in pups of which mother is exposed to this substance at lower doses. However, the mechanism underlying these defects remains to be clarified in spite of many researches conducted so far. Our previous studies have revealed that maternal treatment with TCDD attenuates the production of pituitary gonadotropins [luteinizing hormone (LH) and follicle-stimulating hormone] in the late fetuses, leading to the impairment of sexual behavior in adulthood. To identify the target genes for a fetal reduction in gonadotropin β-subunit, we performed DNA microarray analysis using the fetal pituitary and its regulatory organ, the hypothalamus. The result showed that TCDD induced histone deacetylases (HDACs), and altered the expression of genes including gonadotropin-releasing hormone and activin signaling in the fetal pituitary. Moreover, our data indicated that the increased deacetylation of histone due to HDAC induction plays a critical role for a dioxin-induced attenuation of LHβ in the fetal pituitary. This study suggests a novel molecular mechanism explaining dioxin-produced reproductive toxicity. Pregnant Wistar rats were orally treated with TCDD (1 µg/kg in corn oil) at gestational day (GD)15. Then, the total RNA was extracted from the fetal pituitary and hypothalamus at GD20. To identify the target genes the alteration of which contributes to a reduction in fetal gonadotropin β-subunit, the profile of gene expression was analyzed using the Illumina RatRef-12 Expression BeadChip.
2011-09-30 | E-GEOD-32459 | biostudies-arrayexpress
Project description:Gonadotropin-releasing hormone 3 and gonadotropes relationships in female zebrafish pituitary revealed by single-cell transcriptomics
| PRJNA1138768 | ENA
Project description:We evaluated the efficacy of combining pembrolizumab (anti-PD1 antibody), exemestane (nonsteroidal aromatase inhibitor), and leuprolide (gonadotropin-releasing hormone agonist) for 15 patients with ER+/HER2− premenopausal MBC who had failed one to two lines of hormone therapy without chemotherapy.
2024-10-28 | GSE261815 | GEO