NELF knockout is associated with impaired pubertal development and subfertility
Open accessAbstract
Puberty and reproduction require proper signaling of the hypothalamic-pituitary-gonadal axis controlled by gonadotropin-releasing hormone (GnRH) neurons, which arise in the olfactory placode region and migrate along olfactory axons to the hypothalamus. Factors adversely affecting GnRH neuron specification, migration, and function lead to delayed puberty and infertility. Nasal embryonic luteinizing hormone-releasing factor (NELF) is a predominantly nuclear protein. NELF mutations have been demonstrated in patients with hypogonadotropic hypogonadism, but biallelic mutations are rare and heterozygous NELF mutations typically co-exist with mutations in another gene. Our previous studies in immortalized GnRH neurons supported a role for NELF in GnRH neuron migration. To better understand the physiology of NELF, a homozygous Nelf knockout (KO) mouse model was generated. Our findings indicate that female Nelf KO mice have delayed vaginal opening but no delay in time to first estrus, decreased uterine weight, and reduced GnRH neuron number. In contrast, male mice were normal at puberty. Both sexes of mice had impaired fertility manifested as reduced mean litter size. These data support that NELF has important reproductive functions. The milder than expected phenotype of KO mice also recapitulates the human phenotype since heterozygous NELF mutations usually require an additional mutation in a second gene to result in hypogonadotropic hypogonadism.
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Both NSMF and CHD7 encode proteins known to play a critical developmental role in the GnRH network and have been implicated in patients with pubertal failure (Kallmann syndrome or idiopathic hypogonadotropic hypogonadism).
“Both NSMF (57) and CHD7 (37) encode proteins that are known to play a critical developmental role in the GnRH network and have been implicated in patients with pubertal failure (Kallmann syndrome or idiopathic hypogonadotropic hypogonadism) (36).”
From Functional Hypogonadotropic Hypogonadism in Men: Underlying Neuroendocrine Mechanisms and Natural History (2019) · cites this paper as [57]
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- Authors
- Quaynor, S. D., Ko, E. K., Chorich, L. P., Sullivan, M. E., Demir, D., Waller, J. L., Kim, H.-G., Cameron, R. S., & Layman, L. C.
- Affiliations
- Augusta University (US)
- Corresponding author
- Layman, Lawrence C.
- Venue
- Molecular and Cellular Endocrinology
- Publisher
- Elsevier BV
- Published
- 2015-05
- Volume
- 407
- Pages
- 26-36
- ISSN
- 0303-7207 (ISSN-L)
- PMC
- PMC4429764
- OpenAlex
- W2078231726
- Cited by
- 20
- References
- 51
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 1 · 2021: 2 · 2019: 3 · 2018: 6 · 2017: 3 · 2016: 2 · 2015: 1
- FWCI
- 4.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (RO1 HD033004, RO1HD033004-15)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Reproductive Biology and Fertility
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- NELF, gonadotropin-releasing hormone, delayed puberty, subfertility, hypogonadotropic hypogonadism, GnRH neurons, GnRH neuron migration, hypothalamic-pituitary-gonadal axis, olfactory placode, uterine weight, litter size, sex differences in fertility
- MeSH terms
- Animals, Cell Count, Cell Movement, Estrus, Female, Gene Expression Regulation, Homozygote, Humans, Hypothalamo-Hypophyseal System, Infertility, Gonadotropin-Releasing Hormone, Litter Size, Male, Neurons, Reproduction, Sexual Maturation, Transcription Factors, Uterus, Signal Transduction, Mice, Knockout, Mice
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