Differential regulation of gonadotropins as revealed by transcriptomes of distinct LH and FSH cells of fish pituitary
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ABSTRACT:
PROVIDER: PRJNA669015 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12818264.fastq.gz | Fastqsanger.gz | |||
| SRR12818265.fastq.gz | Fastqsanger.gz | |||
| SRR12818266.fastq.gz | Fastqsanger.gz | |||
| SRR12818267.fastq.gz | Fastqsanger.gz | |||
| SRR12818268.fastq.gz | Fastqsanger.gz |
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Project description:From mammals to fish, gametogenesis and sexual maturation are driven by luteinizing hormone (LH) and follicle-stimulating hormone (FSH), the gonadotropic hormones temporally secreted from the pituitary. Teleost fish are an excellent model for addressing the unique regulation and function of each gonadotropin cell because, unlike mammals, they synthesize and secrete LH and FSH from distinct cells. Only two very distant vertebrate classes (fish and birds), demonstrate the mono-hormonal strategy suggesting a potential convergent evolution. By performing cell specific transcriptome analysis of double-labelled transgenic Nile tilapia (Oreochromis niloticus) expressing GFP and RFP in LH or FSH cells, respectively, we identified genes specifically enriched in each cell type, revealing differences in hormone regulation, receptors expression, cell signaling, and electrical properties. We found that each LH and FSH cell in fish express unique GPCR signature that reveals the direct regulation of metabolic and homeostatic hormones. Comparing these novel transcriptomes to that of rat gonadotrophs revealed conserved genes that might specifically contribute to each gonadotropin activity in mammals, suggesting conserved mechanisms controlling the differential regulation of gonadotropins in vertebrates.
2020-10-14 | GSE159470 | GEO
Project description:In all vertebrates, the dual function of testis (production of sexual steroids and production of gametes) is mainly regulated by two gonadotropic pituitary hormones, FSH and LH. However, in fish the biological activities of the two hormones are not still clearly delineated and moreover, their molecular mechanisms are yet poorly understood. In this study we investigated the effects of FSH and LH on testicular gene expression, in the rainbow trout, at two developmental stages I-II and III (I: spermatogonia only, II: active spermatogonia proliferation, III: meiosis onset with the appearance of spermatocytes and round spermatids). Testes were collected from all-male population rainbow trout and incubated in six replicates for 96 hours, at 12°C, in the absence or presence of purified salmonid gonadotropins, FSH and LH (500 ng/mL).
2012-10-22 | E-GEOD-39465 | biostudies-arrayexpress
Project description:Gonadotropin-releasing hormone (GnRH) governs reproduction in vertebrates by regulating pituitary gonadotropins. Zebrafish, however, is an exception as gnrh3–/– fish, which lack the hypophysiotropic GnRH3, are fertile, suggesting that zebrafish utilizes a Gnrh-independent mechanism to regulate reproduction. To elucidate the role of Gnrh3 and the Gnrh-independent mechanisms that regulate the pituitary gonadotropes, we profiled the gene expression in individual pituitary cells of wild-type and gnrh–/– adult female zebrafish and identified transcriptionally defined cell types. The classical Lh and Fsh gonadotropes expressed both gonadotropin beta subunits with a ratio of 13:1 (lhb:fshb) and 40:1 (fshb:lhb), respectively. We discovered that Lh gonadotropes predominantly express genes encoding receptors for Gnrh (gnrhr2), thyroid hormone, estrogen, dopamine, and steroidogenic factor 1 (SF1). No Gnrh receptor expression was enriched in Fsh gonadotropes, instead, the expression of cholecystokinin receptor (cckrb) and galanin receptor (gal1rb) were enriched in these cells. The hereditary loss of Gnrh3 gene resulted in downregulation of fshb in Lh gonadotropes. Likewise, targeted chemogenetic ablation of Gnrh3 neurons led to a decrease in the number of fshb+/lhb+ cells. Our studies suggest that Gnrh3 directly acts on Lh gonadotropes through Gnrhr2, but the outcome of this interaction is still unknown. Gnrh3 also regulates fshb expression, probably via a non-Gnrh receptor route. Altogether, while Lh secretion and synthesis are likely regulated by multiple factors in a Gnrh-independent manner, Gnrh3 seems to play a role in the cellular organization of the pituitary in zebrafish.
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Project description:We recently demonstrated that Fsh modifies in vitro the testicular transcriptome of rainbow trout at early stages of spermatogenesis. Some of the regulated genes were found related to pathways highly relevant for the testicular functions i.e. spermatogenesis and steroidogenesis. Unlike in mammals, in fish both gonadotropins are able to efficiently stimulate the steroidogenesis, likely through a direct interaction with their cognate receptors present on the Leydig cells. In this context, we wondered whether the effects of Fsh on the tubular compartment were mediated through the production of steroids. To address this issue we performed in vitro incubations of testis explants in the presence of Fsh alone or in combination with an inhibitor of the steroidogenesis, the trilostane. Trilostane significantly reduced or suppressed the response to Fsh of many genes showing that important aspects of the Fsh action on fish testis is indirect and requires the production of steroids. Interestingly, most of the genes regulated in response to Fsh through the steroid mediation were similarly regulated by Lh and many were also found regulated by androgen treatment. On the other hand, for many other genes the response to Fsh was not affected in the presence of trilostane. A majority of those genes were also preferentially regulated by Fsh, as compared to Lh, suggesting that specific regulatory effects of Fsh were independent of steroid production. Finally antagonistic effects between Fsh and steroids were found, in particular for genes encoding clue factors of steroidogenesis or for genes of the Igf system that tended to be inhibited by androgens.
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Project description:We recently demonstrated that Fsh modifies in vitro the testicular transcriptome of rainbow trout at early stages of spermatogenesis. Some of the regulated genes were found related to pathways highly relevant for the testicular functions i.e. spermatogenesis and steroidogenesis. Unlike in mammals, in fish both gonadotropins are able to efficiently stimulate the steroidogenesis, likely through a direct interaction with their cognate receptors present on the Leydig cells. In this context, we wondered whether the effects of Fsh on the tubular compartment were mediated through the production of steroids. To address this issue we performed in vitro incubations of testis explants in the presence of Fsh alone or in combination with an inhibitor of the steroidogenesis, the trilostane. Trilostane significantly reduced or suppressed the response to Fsh of many genes showing that important aspects of the Fsh action on fish testis is indirect and requires the production of steroids. Interestingly, most of the genes regulated in response to Fsh through the steroid mediation were similarly regulated by Lh and many were also found regulated by androgen treatment. On the other hand, for many other genes the response to Fsh was not affected in the presence of trilostane. A majority of those genes were also preferentially regulated by Fsh, as compared to Lh, suggesting that specific regulatory effects of Fsh were independent of steroid production. Finally antagonistic effects between Fsh and steroids were found, in particular for genes encoding clue factors of steroidogenesis or for genes of the Igf system that tended to be inhibited by androgens. Testes were collected from all-male population rainbow trout at early stages of spermatogenesis.Testes were chopped in small pieces, in sterile conditions and then pooled and mixed. Testis fragments were randomly distributed (60-80 mg per well) on Nunc polycarbonate membrane inserts in 24-well plates filled with 300 µL of modified L15 culture medium supplemented with 2% Ultroser SF. Incubation were performed in six replicates for 96 hours, at 12°C, in the absence or presence of purified trout Fsh alone (500 ng/mL) or in combination with 10 µg/mL trilostane, an inhibitor of 3 beta-hydroxysteroid dehydrogenase. A pre-incubation with trilostane was done for 1 hour before adding Fsh.
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Project description:In all vertebrates, the dual function of testis (production of sexual steroids and production of gametes) is mainly regulated by two gonadotropic pituitary hormones, FSH and LH. However, in fish the biological activities of the two hormones are not still clearly delineated and moreover, their molecular mechanisms are yet poorly understood. In this study we investigated the effects of FSH and LH on testicular gene expression, in the rainbow trout, at two developmental stages I-II and III (I: spermatogonia only, II: active spermatogonia proliferation, III: meiosis onset with the appearance of spermatocytes and round spermatids).
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Project description:The Foxo transcription factors regulate multiple cellular functions. Foxo1 and Foxo3 are highly expressed in granulosa cells of ovarian follicles. Selective depletion of the Foxo1 and Foxo3 genes in granulosa cells revealed a novel ovarian-pituitary endocrine feedback loop characterized by: 1) undetectable levels of serum FSH but not LH, 2) reduced expression of the pituitary Fshb gene and its transcriptional regulators and 3) ovarian production of a factor(s) that suppresses pituitary cell Fshb. Equally notable and independent of FSH, depletion of Foxo1/3 altered the expression of specific genes associated with follicle growth versus apoptosis by disrupting critical regulatory interactions of Foxo1/3 with the activin and BMP2 pathways, respectively. As a consequence, granulosa cell proliferation and apoptosis were decreased. These data provide the first evidence that Foxo1/3 divergently regulate follicle growth or death by interacting with the activin and BMP pathways in granulosa cells and by modulating pituitary FSH production. A direct comparison of ovarian granulosa cells from wild type d25, Foxo1/3 dKO d25 and Foxo1/3 dKO 2 month mice.
2013-02-16 | E-GEOD-35593 | biostudies-arrayexpress
Project description:The Foxo transcription factors regulate multiple cellular functions. Foxo1 and Foxo3 are highly expressed in granulosa cells of ovarian follicles. Selective depletion of the Foxo1 and Foxo3 genes in granulosa cells revealed a novel ovarian-pituitary endocrine feedback loop characterized by: 1) undetectable levels of serum FSH but not LH, 2) reduced expression of the pituitary Fshb gene and its transcriptional regulators and 3) ovarian production of a factor(s) that suppresses pituitary cell Fshb. Equally notable and independent of FSH, depletion of Foxo1/3 altered the expression of specific genes associated with follicle growth versus apoptosis by disrupting critical regulatory interactions of Foxo1/3 with the activin and BMP2 pathways, respectively. As a consequence, granulosa cell proliferation and apoptosis were decreased. These data provide the first evidence that Foxo1/3 divergently regulate follicle growth or death by interacting with the activin and BMP pathways in granulosa cells and by modulating pituitary FSH production.
2013-02-16 | GSE35593 | GEO
Project description:Effects of the absence of a functional LH receptor and/or expression of a constitutively active FSH receptor on gene expression in the gonads of male mice were studied. The results provide insights into the roles of the hormones LH and FSH in male reproduction. The main conclusion is that constant strong FSH stimulation is able to rescue the impaired spermatogenesis and fertility of male mice in the absence of LH signalling.
2016-01-20 | GSE76945 | GEO
Project description:Inter-organ communication is a major hallmark of health and is often orchestrated by hormones released by the anterior pituitary gland. Pituitary gonadotropes secrete follicle-stimulating hormone (FSH) and luteinizing hormone (LH) to regulate gonadal function and control fertility. Whether FSH and LH also act on organs other than the gonads is debated. Here, we found that gonadotrope depletion in adult female mice triggers profound hypogonadism, obesity, glucose intolerance, fatty liver, and bone loss. The absence of sex steroids precipitates these phenotypes, with the notable exception of fatty liver, which results from ovary-independent actions of FSH. We uncover paracrine FSH action on pituitary corticotropes as a novel mechanism to restrain the production of corticosterone and prevent hepatic steatosis. Our data demonstrate that functional communication of two distinct hormone-secreting cell populations in the pituitary regulates hepatic lipid metabolism.
2023-01-11 | GSE216096 | GEO