Regulation of gonadotropin subunit gene transcription

Burger, Laura L.; Haisenleder, Daniel J.; Dalkin, Alan C.; Marshall, John C.

doi:10.1677/jme.1.01600

Cited by 172 publications

(140 citation statements)

References 194 publications

(207 reference statements)

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“…Similar to those in mammals (Gharib et al 1990, Burger et al 2004, the secretion and expression of fish gonadotropins are controlled by both neuroendocrine factors from the hypothalamus such as gonadotropin-releasing hormone (GnRH; Peter et al 1986, Weltzien et al 2004, Ando & Urano 2005 and steroids from the gonads (Kobayashi et al 1987, Dickey & Swanson 1998. Our previous study in the goldfish demonstrated that in addition to the neuroendocrine and endocrine regulation, pituitary gonadotropins are also subject to local paracrine regulation by activin (Yam et al 1999a, Yuen & Ge 2004, similar to the situation in mammals (Roberts et al 1989, Corrigan et al 1991, Bilezikjian et al 2004.…”

Section: Introductionmentioning

confidence: 80%

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Cheng¹,

Yuen²,

Ge³

2007

Journal of Endocrinology

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Activin is an important regulator of gonadotropin expression and production in the vertebrate pituitary, and its activity is fine-tuned by its binding protein follistatin. In the present study, a full-length cDNA for follistatin was cloned in the goldfish, which shows 74% amino acid sequence identity with that of mammals. Recombinant goldfish follistatin expressed in the Chinese hamster ovary cells significantly blocked activin-induced F5-5 cell differentiation. Goldfish follistatin is expressed in a wide range of tissues including the brain, pituitary, ovary, and testis. The expression of follistatin mRNA in the pituitary is regulated by both activin and gonadal steroids in vitro. Treatment with goldfish activin B for 48 h significantly up-regulated follistatin expression in cultured pituitary cells, suggesting a closed activin-follistatin feedback loop in the pituitary. In agreement with this, both human and goldfish follistatin down-regulated the expression of follistatin itself, probably due to the neutralization of endogenous activin. Examination of FSHb and LHb expression in the same samples supports the role of activin and follistatin in the differential regulation of FSH and LH as demonstrated previously. Since the expression level of activin b B in the pituitary is rather stable both in vitro and in vivo, it is conceivable that follistatin may play a pivotal regulatory role in the intra-pituitary activin system. Both estradiol and testosterone up-regulated follistatin expression in vitro, suggesting a mediating role for follistatin in steroid feedback on pituitary hormones. These results provide clues to the potential physiological roles of activin-follistatin system in the regulation of gonadotropin biosynthesis in teleosts.

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Section: Introductionmentioning

confidence: 80%

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Cheng¹,

Yuen²,

Ge³

2007

Journal of Endocrinology

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“…The consequences of modifying these secretion pathways have not been tested in vivo. In the pituitary, GnRH pulse characteristics are critical for differential regulation of LH and FSH (30)(31)(32)(33). Emerging evidence suggests GnRH pulses are interpreted at the level of gonadotropin β-subunit promoters, downstream signaling cascades involving MAPKs and ultimately reflected in corresponding subunit biosynthesis (31,33).…”

Section: Discussionmentioning

confidence: 99%

Redirecting intracellular trafficking and the secretion pattern of FSH dramatically enhances ovarian function in mice

Wang¹,

Larson²,

Jablonka‐Shariff

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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FSH and luteinizing hormone (LH) are secreted constitutively or in pulses, respectively, from pituitary gonadotropes in many vertebrates, and regulate ovarian function. The molecular basis for this evolutionarily conserved gonadotropin-specific secretion pattern is not understood. Here, we show that the carboxyterminal heptapeptide in LH is a gonadotropin-sorting determinant in vivo that directs pulsatile secretion. FSH containing this heptapeptide enters the regulated pathway in gonadotropes of transgenic mice, and is released in response to gonadotropin-releasing hormone, similar to LH. FSH released from the LH secretory pathway rescued ovarian defects in Fshb-null mice as efficiently as constitutively secreted FSH. Interestingly, the rerouted FSH enhanced ovarian follicle survival, caused a dramatic increase in number of ovulations, and prolonged female reproductive lifespan. Furthermore, the rerouted FSH vastly improved the in vivo fertilization competency of eggs, their subsequent development in vitro and when transplanted, the ability to produce offspring. Our study demonstrates the feasibility to fine-tune the target tissue responses by modifying the intracellular trafficking and secretory fate of a pituitary trophic hormone. The approach to interconvert the secretory fate of proteins in vivo has pathophysiological significance, and could explain the etiology of several hormone hyperstimulation and resistance syndromes.protein sorting | regulated secretion | dense core granules | folliculogenesis

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“…The synthesis of gonadotropin subunits in the anterior pituitary is mainly stimulated by gonadotropin-releasing hormone (GnRH) secreted from neurons which extend to the pituitary by way of the hypothalamus (15)(16)(17)(18)(19). GnRH binds to its specific receptor on the membrane of pituitary gonadotropes, and activates several signaling pathways involving PKC, PKA, MAPKs, and calcium/calmodulin-dependent protein kinases (16).…”

mentioning

confidence: 99%

“…GnRH binds to its specific receptor on the membrane of pituitary gonadotropes, and activates several signaling pathways involving PKC, PKA, MAPKs, and calcium/calmodulin-dependent protein kinases (16). The activated kinases modulate the action of transcription factors and repressors located downstream to regulate the expression of gonadotropins in a subunit-specific manner (17)(18)(19). Our recent study has suggested that TCDD suppresses GnRH-mediated PKC and PKA and/or their downstream mechanisms in cultivated fetal pituitary to attenuate gonadotropin synthesis (20).…”

mentioning

confidence: 99%

Dioxin Silences Gonadotropin Expression in Perinatal Pups by Inducing Histone Deacetylases

Takeda

Fujii

Taura

et al. 2012

Journal of Biological Chemistry

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Background: Dioxin attenuates the fetal production of luteinizing hormone (LH) to imprint impaired sexual behavior. Results: Fetal exposure to dioxin induces histone deacetylases to attenuate the acetylation status of histones twisted around the LH␤ gene. Conclusion: Histone deacetylation in the pituitary contributes to the dioxin-induced damage to fetal/infant steroidogenesis. Significance: This study provides a new insight into the mechanism underlying sexual immaturity caused by dioxin.

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Regulation of gonadotropin subunit gene transcription

Cited by 172 publications

References 194 publications

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Evidence for the existence of a local activin–follistatin negative feedback loop in the goldfish pituitary and its regulation by activin and gonadal steroids

Redirecting intracellular trafficking and the secretion pattern of FSH dramatically enhances ovarian function in mice

Dioxin Silences Gonadotropin Expression in Perinatal Pups by Inducing Histone Deacetylases

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