Differential regulation of follicle stimulating hormone by activin A and TGFB1 in murine gonadotropes

Gore, A. Jesse; Philips, Daniel P; Miller, William L.; Bernard, Daniel J.

doi:10.1186/1477-7827-3-73

Cited by 20 publications

(4 citation statements)

References 87 publications

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“…TGFBR3L enables inhibin B to act with high affinity and without competition by other TGFβ family members. Murine gonadotropes do not express the TGFβ type II receptor and therefore cannot transduce signals by TGFβs ( 50 , 51 ). However, TGFβs can still bind betaglycan in this context and thereby competitively antagonize inhibin A (and presumably inhibin B) actions ( 52 , 53 ).…”

Section: Discussionmentioning

confidence: 99%

TGFBR3L is an inhibin B co-receptor that regulates female fertility

Brûlé

Wang

et al. 2021

Sci. Adv.

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Section: Discussionmentioning

confidence: 99%

TGFBR3L is an inhibin B co-receptor that regulates female fertility

Brûlé

Wang

et al. 2021

Sci. Adv.

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“…FOXL2 and ESR1 potential regulatory elements identified from ChIP-Seq were amplified from primary follicle cell genomic DNA and inserted between the KpnI and NheI sites of the pGL3-promoter vector (Promega, Madison, Wisconsin). Vectors driving the expression of FOXL2, SMAD3 have been described previously ( Anttonen et al, 2014 ), and the vector expressing constitutively active TGFBR1 (with T204D mutation) was a kind gift of Dr Peter Scheiffele ( Gore et al, 2005 ).…”

Section: Methodsmentioning

confidence: 99%

The transcription factor FOXL2 mobilizes estrogen signaling to maintain the identity of ovarian granulosa cells

Georges

L’Hôte

Todeschini

et al. 2014

eLife

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FOXL2 is a lineage determining transcription factor in the ovary, but its direct targets and modes of action are not fully characterized. In this study, we explore the targets of FOXL2 and five nuclear receptors in murine primary follicular cells. We found that FOXL2 is required for normal gene regulation by steroid receptors, and we show that estrogen receptor beta (ESR2) is the main vector of estradiol signaling in these cells. Moreover, we found that FOXL2 directly modulates Esr2 expression through a newly identified intronic element. Interestingly, we found that FOXL2 repressed the testis-determining gene Sox9 both independently of estrogen signaling and through the activation of ESR2 expression. Altogether, we show that FOXL2 mobilizes estrogen signaling to establish a coherent feed-forward loop repressing Sox9. This sheds a new light on the role of FOXL2 in ovarian maintenance and function.DOI: http://dx.doi.org/10.7554/eLife.04207.001

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“…Fshb expression is induced by activin [ 46 ]. Activin A and activin B are homodimers of the inhibin βA (Inhba) or inhibin βB (INHBB) subunits, respectively.…”

Section: Resultsmentioning

confidence: 99%

Maximal Expression of Foxl2 in Pituitary Gonadotropes Requires Ovarian Hormones

Herndon

Nilson

2015

PLoS ONE

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Gonadotropin-releasing hormone (GnRH) and activin regulate synthesis of FSH and ultimately fertility. Recent in vivo studies cast SMAD4 and FOXL2 as master transcriptional mediators of activin signaling that act together and independently of GnRH to regulate Fshb gene expression and female fertility. Ovarian hormones regulate GnRH and its receptor (GNRHR) through negative and positive feedback loops. In contrast, the role of ovarian hormones in regulating activin, activin receptors, and components of the activin signaling pathway, including SMAD4 and FOXL2, remains understudied. The widespread distribution of activin and many of its signaling intermediates complicates analysis of the effects of ovarian hormones on their synthesis in gonadotropes, one of five pituitary cell types. We circumvented this complication by using a transgenic model that allows isolation of polyribosomes selectively from gonadotropes of intact females and ovariectomized females treated with or without a GnRH antagonist. This paradigm allows assessment of ovarian hormonal feedback and distinguishes responses that are either independent or dependent on GnRH. Surprisingly, our results indicate that Foxl2 levels in gonadotropes decline significantly in the absence of ovarian input and independently of GnRH. Expression of the genes encoding other members of the activin signaling pathway are unaffected by loss of ovarian hormonal feedback, highlighting their selective effect on Foxl2. Expression of Gnrhr, a known target of FOXL2, also declines upon ovariectomy consistent with reduced expression of Foxl2 and loss of ovarian hormones. In contrast, Fshb mRNA increases dramatically post-ovariectomy due to increased compensatory input from GnRH. Together these data suggest that ovarian hormones regulate expression of Foxl2 thereby expanding the number of genes controlled by the hypothalamic-pituitary-gonadal axis that ultimately dictate reproductive fitness.

show abstract

Differential regulation of follicle stimulating hormone by activin A and TGFB1 in murine gonadotropes

Cited by 20 publications

References 87 publications

TGFBR3L is an inhibin B co-receptor that regulates female fertility

TGFBR3L is an inhibin B co-receptor that regulates female fertility

The transcription factor FOXL2 mobilizes estrogen signaling to maintain the identity of ovarian granulosa cells

Maximal Expression of Foxl2 in Pituitary Gonadotropes Requires Ovarian Hormones

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