Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Tsai, Pei‐San; Brooks, Leah; Rochester, Johanna R.; Kavanaugh, Scott I.; Chung, Wilson C.J.

doi:10.1016/j.yfrne.2010.11.002

Cited by 42 publications

(41 citation statements)

References 152 publications

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“…+ collar progenitors Emerging studies from a number of vertebrates suggest that FGF signalling plays a pivotal role in development of the neuroendocrine hypothalamus and the pituitary gland, and raise the notion that FGFs might govern the development of the infundibulum itself, potentially via effects on proliferation (for a review, see Tsai et al, 2011). Our studies suggest a mechanism for FGF function in infundibular growth, showing that FGF signalling is necessary for the proliferation of collar cells.…”

Section: Fgf Signalling Governs Proliferating Sox3mentioning

confidence: 55%

“…In all vertebrates examined, FGFs are expressed within both fpderived cells of the ventral hypothalamic midline (Manning et al, 2006) and the forming infundibulum (Tannahill et al, 1992;Ohuchi et al, 2000;Herzog et al, 2004;Theil et al, 2008;Tsai et al, 2011), where they may play multiple roles in the neuroendocrine hypothalamus. FGFs act as spatial and proliferative cues for progenitors within Rathke's pouch, which is the precursor of the anterior pituitary (Ericson et al, 1998;Norlin et al, 2000;Zhu et al, 2007), and additionally promote diverse aspects of specification of neuroendocrine neurons (Tsai et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

“…FGFs act as spatial and proliferative cues for progenitors within Rathke's pouch, which is the precursor of the anterior pituitary (Ericson et al, 1998;Norlin et al, 2000;Zhu et al, 2007), and additionally promote diverse aspects of specification of neuroendocrine neurons (Tsai et al, 2011). Similarly, emerging evidence supports a function for FGF signalling in development of the infundibulum itself.…”

Section: Introductionmentioning

confidence: 99%

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FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

et al. 2011

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SUMMARYThe infundibulum links the nervous and endocrine systems, serving as a crucial integrating centre for body homeostasis. Here we describe that the chick infundibulum derives from two subsets of anterior ventral midline cells. One set remains at the ventral midline and forms the posterior-ventral infundibulum. A second set migrates laterally, forming a collar around the midline. We show that collar cells are composed of Fgf3 + SOX3 + proliferating progenitors, the induction of which is SHH dependent, but the maintenance of which requires FGF signalling. Collar cells proliferate late into embryogenesis, can generate neurospheres that passage extensively, and differentiate to distinct fates, including hypothalamic neuronal fates and Fgf10 + anterior-dorsal infundibular cells. Together, our study shows that a subset of anterior floor plate-like cells gives rise to Fgf3 + SOX3 + progenitor cells, demonstrates a dual origin of infundibular cells and reveals a crucial role for FGF signalling in governing extended infundibular growth.

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Section: Fgf Signalling Governs Proliferating Sox3mentioning

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

et al. 2011

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“…Several studies have elucidated important roles for Shh, BMP, Wnt, FGF and Nodal signaling in proper patterning of the posterior hypothalamus and the development of the hypothalamic progenitors Kapsimali et al, 2004;Lee et al, 2006;Manning et al, 2006;Mathieu et al, 2002;Ohyama et al, 2008;Pearson et al, 2011;Tsai et al, 2011;Wang et al, 2012). However, downstream factors that contribute to posterior hypothalamic neuronal specification are not well understood.…”

Section: Introductionmentioning

confidence: 99%

Specification of posterior hypothalamic neurons requires coordinated activities of Fezf2, Otp, Sim1a and Foxb1.2

Wolf

Ryu

2013

Development

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SUMMARYThe hypothalamus is a key integrative center in the brain that consists of diverse cell types required for a variety of functions including homeostasis, reproduction, stress response, social and cognitive behavior. Despite our knowledge of several transcription factors crucial for hypothalamic development, it is not known how the wide diversity of neuron types in the hypothalamus is produced. In particular, almost nothing is known about the mechanisms that specify neurons in the posteriormost part of the hypothalamus, the mammillary area. Here, we investigated the specification of two distinct neuron types in the mammillary area that produce the hypothalamic hormones Vasoactive intestinal peptide (Vip) and Urotensin 1 (Uts1). We show that Vip-and Uts1-positive neurons develop in distinct domains in the mammillary area defined by the differential expression of the transcription factors Fezf2, Otp, Sim1a and Foxb1.2. Coordinated activities of these factors are crucial for the establishment of the mammillary area subdomains and the specification of Vip-and Uts1-positive neurons. In addition, Fezf2 is important for early development of the posterior hypothalamus. Thus, our study provides the first molecular anatomical map of the posterior hypothalamus in zebrafish and identifies, for the first time, molecular requirements underlying the specification of distinct posterior hypothalamic neuron types.

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“…It has been shown that fibroblast growth factor (FGF) signaling is critical to the formation of a functional GnRH system in humans [5,6] and rodents [7]. An interesting convergence between humans and rodents is the dependence of both models on Fgf receptor 1 (Fgfr1) and Fgf8 to support GnRH neuronal development [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Fibroblast Growth Factor Signaling Deficiencies Impact Female Reproduction and Kisspeptin Neurons in Mice1

Tata¹,

Chung²,

Brooks³

et al. 2012

Biology of Reproduction

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Fibroblast growth factor (FGF) signaling is essential for the development of the gonadotropin-releasing hormone (GnRH) system. Mice harboring deficiencies in Fgf8 or Fgf receptor 1 (Fgfr1) suffer a significant loss of GnRH neurons, but their reproductive phenotypes have not been examined. This study examined if female mice hypomorphic for Fgf8, Fgfr1, or both (compound hypomorphs) exhibited altered parameters of pubertal onset, estrous cyclicity, and fertility. Further, we examined the number of kisspeptin (KP)-immunoreactive (ir) neurons in the anteroventral periventricular/periventricular nuclei (AVPV/PeV) of these mice to assess if changes in the KP system, which stimulates the GnRH system, could contribute to the reproductive phenotypes. Single hypomorphs (Fgfr1(+/-) or Fgf8(+/-)) had normal timing for vaginal opening (VO) but delayed first estrus. However, after achieving the first estrus, they underwent normal expression of estrous cycles. In contrast, the compound hypomorphs underwent early VO and normal first estrus, but had disorganized estrous cycles that subsequently reduced their fertility. KP immunohistochemistry on Postnatal Day 15, 30, and 60 transgenic female mice revealed that female compound hypomorphs had significantly more KP-ir neurons in the AVPV/PeV compared to their wild-type littermates, suggesting increased KP-ir neurons may drive early VO but could not maintain the cyclic changes in GnRH neuronal activity required for female fertility. Overall, these data suggest that Fgf signaling deficiencies differentially alter the parameters of female pubertal onset and cyclicity. Further, these deficiencies led to changes in the AVPV/PeV KP-ir neurons that may have contributed to the accelerated VO in the compound hypomorphs.

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Fibroblast growth factor signaling in the developing neuroendocrine hypothalamus

Cited by 42 publications

References 152 publications

FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

FGF-dependent midline-derived progenitor cells in hypothalamic infundibular development

Specification of posterior hypothalamic neurons requires coordinated activities of Fezf2, Otp, Sim1a and Foxb1.2

Fibroblast Growth Factor Signaling Deficiencies Impact Female Reproduction and Kisspeptin Neurons in Mice1

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