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TAC3 and TACR3 mutations in familial hypogonadotropic hypogonadism reveal a key role for Neurokinin B in the central control of reproduction
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TAC3 and TACR3 mutations in familial hypogonadotropic hypogonadism reveal a key role for Neurokinin B in the central control of reproduction
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Journal Article
TAC3 and TACR3 mutations in familial hypogonadotropic hypogonadism reveal a key role for Neurokinin B in the central control of reproduction
2009
Overview
A. Kemal Topaloglu and colleagues report the identification of mutations in the neurokinin B receptor and its ligand in families with severe congenital gonadotropin deficiency and pubertal failure. These findings indicate that neurokinin B is a central regulator of human gonadal function.
The timely secretion of gonadal sex steroids is essential for the initiation of puberty, the postpubertal maintenance of secondary sexual characteristics and the normal perinatal development of male external genitalia. Normal gonadal steroid production requires the actions of the pituitary-derived gonadotropins, luteinizing hormone and follicle-stimulating hormone. We report four human pedigrees with severe congenital gonadotropin deficiency and pubertal failure in which all affected individuals are homozygous for loss-of-function mutations in
TAC3
(encoding Neurokinin B) or its receptor
TACR3
(encoding NK3R). Neurokinin B, a member of the substance P–related tachykinin family, is known to be highly expressed in hypothalamic neurons that also express kisspeptin
1
, a recently identified regulator of gonadotropin-releasing hormone secretion
2
. These findings implicate Neurokinin B as a critical central regulator of human gonadal function and suggest new approaches to the pharmacological control of human reproduction and sex hormone-related diseases.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animal Genetics and Genomics
/ Biological and medical sciences
/ Biomedical and Life Sciences
/ Family
/ Fundamental and applied biological sciences. Psychology
/ Genetics
/ Genetics of eukaryotes. Biological and molecular evolution
/ Gonadotropin releasing hormone
/ Humans
/ Hypothalamus. Hypophysis. Epiphysis (diseases)
/ letter
/ Mutation
/ Non tumoral diseases. Target tissue resistance. Benign neoplasms
/ Pedigree
/ Puberty
/ Receptors, Neurokinin-3 - genetics
/ Receptors, Neurokinin-3 - metabolism
/ Sequence Homology, Amino Acid
/ Steroids
