Pharyngeal pituitary: development, malformation, and tumorigenesis

1999 ◽  
Vol 98 (3) ◽  
pp. 262-272 ◽  
Author(s):  
A. Hori ◽  
D. Schmidt ◽  
E. Rickels
Keyword(s):  
Pituitary Development ◽  
Pharyngeal Pituitary

Transcriptional Regulation in Mammalian Pituitary Development and Disease

2001 ◽  
Vol 2 (4) ◽  
pp. 379-397 ◽  
Author(s):  
Kyle Sloop ◽  
Gretchen Parker ◽  
Simon Rhodes
Keyword(s):  
Transcriptional Regulation ◽  
Pituitary Development

scholarly journals Homeodomain Proteins SIX3 and SIX6 Regulate Gonadotrope-specific Genes During Pituitary Development

2015 ◽  
Vol 29 (6) ◽  
pp. 842-855 ◽  
Author(s):  
Huimin Xie ◽  
Hanne M. Hoffmann ◽  
Jason D. Meadows ◽  
Susan L. Mayo ◽  
Crystal Trang ◽  
...  
Keyword(s):  
Homeodomain Proteins ◽  
Pituitary Development

A mutation of the β-domain in POU1F1 causes pituitary deficiency due to dominant PIT-1β expression

2021 ◽  
Author(s):  
Shigeru Suzuki ◽  
Kumihiro Matsuo ◽  
Yoshiya Ito ◽  
Atsushi Kobayashi ◽  
Takahide Kokumai ◽  
...  
Keyword(s):  
Hormone Deficiency ◽  
Luciferase Reporter ◽  
Heterozygous Mutation ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Transactivation Domain ◽  
Exon 2 ◽  
Pituitary Development ◽  
Long Term Follow Up ◽  
Alternatively Spliced

Background: POU1F1 encodes both PIT-1α, which plays pivotal roles in pituitary development and GH, PRL and TSHB expression, and the alternatively spliced isoform PIT-1β, which contains an insertion of 26-amino acids (β-domain) in the transactivation domain of PIT-1α due to the use of an alternative splice acceptor at the end of the first intron. PIT-1β is expressed at much lower levels than PIT-1α and represses endogenous PIT-1α transcriptional activity. Although POU1F1 mutations lead to combined pituitary hormone deficiency (CPHD), no patients with β-domain mutations have been reported. Results: Here, we report that a three-generation family exhibited different degrees of CPHD, including growth hormone deficiency with intrafamilial variability of prolactin/TSH insufficiency and unexpected prolactinoma occurrence. The CPHD was due to a novel POU1F1 heterozygous variant (c.143-69T>G) in intron 1 of PIT-1α (RefSeq number NM_000306) or as c.152T>G (p.Ile51Ser) in exon 2 of PIT-1β (NM_001122757). Gene splicing experiments showed that this mutation yielded the PIT-1β transcript without other transcripts. Lymphocyte PIT-1β mRNA expression was significantly higher in the patients with the heterozygous mutation than a control. A luciferase reporter assay revealed that the PIT-1β-Ile51Ser mutant repressed PIT-1α and abolished transactivation capacity for the rat prolactin promoter in GH3 pituitary cells. Conclusions: We describe, for the first time, that PIT-1β mutation can cause CPHD through a novel genetic mechanism, such as PIT-1β overexpression, and that POU1F1 mutation might be associated with a prolactinoma. Analysis of new patients and long-term follow-up are needed to clarify the characteristics of PIT-1β mutations.

The pituitary adrenocorticotropes originate from neural ridge tissue in Xenopus laevis

Development ◽  
1986 ◽  
Vol 95 (1) ◽  
pp. 1-14
Author(s):  
Gerald W. Eagleson ◽  
Bruce G. Jenks ◽  
A. P. van Overbeeke
Keyword(s):  
Xenopus Laevis ◽  
Anterior Pituitary ◽  
Preoptic Region ◽  
Anterior Portion ◽  
Pituitary Development ◽  
Immunocytochemical Techniques ◽  
Nucleus Infundibularis ◽  
Tube Closure

A series of grafting experiments was conducted to determine pituitary origins prior to brain tube closure in Xenopus laevis. Extirpation experiments indicated that the ventral neural ridge (VNR) tissue of stage-18+ embryos was essential for pituitary development. Bolton–Hunter reagent was used to label stage-18+ VNR tissue with 125I, and this tissue was then returned to the donor and its subsequent ontogenesis followed. Labelled tissue was ultimately found in the ventral hypothalamus, the ventral retina, and the anterior pituitary. Using immunocytochemical techniques with antisera to adrenocorticotropin (ACTH), it was found that some of the VNR-derived cells were corticotropes. A region of the nucleus infundibularis which was radioactive labelled also gave ACTH-positive immunoreaction. This might indicate that some ACTH containing neurones of the hypothalamus are VNR in origin. We suggest that stage-18+ VNR is the site of attachment of brain and anterior pituitary ectoderm. Part of this adherence point is eventually incorporated into the anterior pituitary and will form corticotropes. It is concluded that the ventral retina, the preoptic region of the hypothalamus, some hypothalamic ACTH-immunoreactive cells, and the most anterior portion of the adenohypophysis are all ventral neural ridge in origin.

Lhx4 and Prop1 are required for cell survival and expansion of the pituitary primordia

Development ◽  
2002 ◽  
Vol 129 (18) ◽  
pp. 4229-4239 ◽  
Author(s):  
Lori T. Raetzman ◽  
Robert Ward ◽  
Sally A. Camper
Keyword(s):  
Cell Survival ◽  
Anterior Pituitary ◽  
Molecular Genetic ◽  
Cell Types ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Pituitary Cells ◽  
Temporal Shift ◽  
Pituitary Development ◽  
Show Evidence

Deficiencies in the homeobox transcription factors LHX4 and PROP1 cause pituitary hormone deficiency in both humans and mice. Lhx4 and Prop1 mutants exhibit severe anterior pituitary hypoplasia resulting from limited differentiation and expansion of most specialized cell types. Little is known about the mechanism through which these genes promote pituitary development. In this study we determined that the hypoplasia in Lhx4 mutants results from increased cell death and that the reduced differentiation is attributable to a temporal shift in Lhx3 activation. In contrast, Prop1 mutants exhibit normal cell proliferation and cell survival but show evidence of defective dorsal-ventral patterning. Molecular genetic analyses reveal that Lhx4 and Prop1 have overlapping functions in early pituitary development. Double mutants exhibit delayed corticotrope specification and complete failure of all other anterior pituitary cell types to differentiate. Thus, Lhx4 and Prop1 have critical, but mechanistically different roles in specification and expansion of specialized anterior pituitary cells.

scholarly journals Myostatin regulates pituitary development and hepatic IGF1

2019 ◽  
Vol 316 (6) ◽  
pp. E1036-E1049 ◽  
Author(s):  
Wioletta Czaja ◽  
Yukiko K. Nakamura ◽  
Naisi Li ◽  
Jennifer A. Eldridge ◽  
David M. DeAvila ◽  
...  
Keyword(s):  
Striated Muscle ◽  
Muscle Growth ◽  
Unintended Consequences ◽  
Pituitary Development ◽  
Igf Binding ◽  
Acid Labile Subunit ◽  
Muscle Wasting Disease ◽  
And Function ◽  
Igf Binding Protein ◽  
Igf1 Expression

Circulating myostatin-attenuating agents are being developed to treat muscle-wasting disease despite their potential to produce serious off-target effects, as myostatin/activin receptors are widely distributed among many nonmuscle tissues. Our studies suggest that the myokine not only inhibits striated muscle growth but also regulates pituitary development and growth hormone (GH) action in the liver. Using a novel myostatin-null label-retaining model (Jekyll mice), we determined that the heterogeneous pool of pituitary stem, transit-amplifying, and progenitor cells in Jekyll mice depletes more rapidly after birth than the pool in wild-type mice. This correlated with increased levels of GH, prolactin, and the cells that secrete these hormones, somatotropes and lactotropes, respectively, in Jekyll pituitaries. Recombinant myostatin also stimulated GH release and gene expression in pituitary cell cultures although inhibiting prolactin release. In primary hepatocytes, recombinant myostatin blocked GH-stimulated expression of two key mediators of growth, insulin-like growth factor (IGF)1 and the acid labile subunit and increased expression of an inhibitor, IGF-binding protein-1. The significance of these findings was demonstrated by smaller muscle fiber size in a model lacking myostatin and liver IGF1 expression (LID-o-Mighty mice) compared with that in myostatin-null (Mighty) mice. These data together suggest that myostatin may regulate pituitary development and function and that its inhibitory actions in muscle may be partly mediated by attenuating GH action in the liver. They also suggest that circulating pharmacological inhibitors of myostatin could produce unintended consequences in these and possibly other tissues.

scholarly journals Developmental Genes and Malformations in the Hypothalamus

2020 ◽  
Vol 14 ◽  
Author(s):  
Carmen Diaz ◽  
Luis Puelles
Keyword(s):  
Transcription Factors ◽  
Energy Metabolism ◽  
Molecular Mechanisms ◽  
Review Article ◽  
Pituitary Development ◽  
Forebrain Development ◽  
Physiological Processes ◽  
Brain Malformations ◽  
Clinical Complexity ◽  
Genes Encoding

The hypothalamus is a heterogeneous rostral forebrain region that regulates physiological processes essential for survival, energy metabolism, and reproduction, mainly mediated by the pituitary gland. In the updated prosomeric model, the hypothalamus represents the rostralmost forebrain, composed of two segmental regions (terminal and peduncular hypothalamus), which extend respectively into the non-evaginated preoptic telencephalon and the evaginated pallio-subpallial telencephalon. Complex genetic cascades of transcription factors and signaling molecules rule their development. Alterations of some of these molecular mechanisms acting during forebrain development are associated with more or less severe hypothalamic and pituitary dysfunctions, which may be associated with brain malformations such as holoprosencephaly or septo-optic dysplasia. Studies on transgenic mice with mutated genes encoding critical transcription factors implicated in hypothalamic-pituitary development are contributing to understanding the high clinical complexity of these pathologies. In this review article, we will analyze first the complex molecular genoarchitecture of the hypothalamus resulting from the activity of previous morphogenetic signaling centers and secondly some malformations related to alterations in genes implicated in the development of the hypothalamus.

HORMONAL CONTENT OF THE PHARYNGEAL PITUITARY GLAND

Endocrinology ◽  
1941 ◽  
Vol 29 (2) ◽  
pp. 228-229 ◽  
Author(s):  
STEPHEN TOLINS ◽  
ROBERT A. MOORE
Keyword(s):  
Pituitary Gland ◽  
Hormonal Content ◽  
Pharyngeal Pituitary

Transcriptional control during mammalian anterior pituitary development

Gene ◽  
2003 ◽  
Vol 319 ◽  
pp. 1-19 ◽  
Author(s):  
Jesse J Savage ◽  
Benjamin C Yaden ◽  
Parinda Kiratipranon ◽  
Simon J Rhodes
Keyword(s):  
Anterior Pituitary ◽  
Transcriptional Control ◽  
Pituitary Development
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