ArticleNature communications2022
Dicer ablation in Kiss1 neurons impairs puberty and fertility preferentially in female mice.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Obesity, Oxidative Stress, and Inflammation in Precocious Puberty: Do All Roads Lead to the Hypothalamus?International journal of molecular sciences · 2026Review
- Hypothalamic control of puberty: from neuronal circuits to mechanisms for its metabolic regulation.Reviews in endocrine & metabolic disorders · 2026Review
- Hypothalamic endoplasmic reticulum stress drives pubertal precocity due to early-onset obesity in female rodents.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Brainstem noradrenergic modulation of the kisspeptin neuron GnRH pulse generator in mice.Nature communications · 2025Article
- Kisspeptin and neurokinin B: roles in reproductive health.Physiological reviews · 2025Review
- GnRH and Cognition.Endocrinology · 2025Review
- Metabolic control of puberty: 60 years in the footsteps of Kennedy and Mitra's seminal work.Nature reviews. Endocrinology · 2024Review
- Molecular basis of normal and pathological puberty: from basic mechanisms to clinical implications.The lancet. Diabetes & endocrinology · 2023Review
- Overexpression of Brain- and Glial Cell Line-Derived Neurotrophic Factors Is Neuroprotective in an Animal Model of Acute Hypobaric Hypoxia.International journal of molecular sciences · 2022Article
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Authors and funding
19 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kiss1 neurons, producing kisspeptins, are essential for puberty and fertility, but their molecular regulatory mechanisms remain unfolded. Here, we report that congenital ablation of the microRNA-synthesizing enzyme, Dicer, in Kiss1 cells, causes late-onset hypogonadotropic hypogonadism in both sexes, but is compatible with pubertal initiation and preserved Kiss1 neuronal populations at the infantile/juvenile period. Yet, failure to complete puberty and attain fertility is observed only in females. Kiss1-specific ablation of Dicer evokes disparate changes of Kiss1-cell numbers and Kiss1/kisspeptin expression between hypothalamic subpopulations during the pubertal-transition, with a predominant decline in arcuate-nucleus Kiss1 levels, linked to enhanced expression of its repressors, Mkrn3, Cbx7 and Eap1. Our data unveil that miRNA-biosynthesis in Kiss1 neurons is essential for pubertal completion and fertility, especially in females, but dispensable for initial reproductive maturation and neuronal survival in both sexes. Our results disclose a predominant miRNA-mediated inhibitory program of repressive signals that is key for precise regulation of Kiss1 expression and, thereby, reproductive function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.