Abstract:
:Puberty is regulated by epigenetic mechanisms and is highly sensitive to metabolic and nutritional cues. However, the epigenetic pathways mediating the effects of nutrition and obesity on pubertal timing are unknown. Here, we identify Sirtuin 1 (SIRT1), a fuel-sensing deacetylase, as a molecule that restrains female puberty via epigenetic repression of the puberty-activating gene, Kiss1. SIRT1 is expressed in hypothalamic Kiss1 neurons and suppresses Kiss1 expression. SIRT1 interacts with the Polycomb silencing complex to decrease Kiss1 promoter activity. As puberty approaches, SIRT1 is evicted from the Kiss1 promoter facilitating a repressive-to-permissive switch in chromatin landscape. Early-onset overnutrition accelerates these changes, enhances Kiss1 expression and advances puberty. In contrast, undernutrition raises SIRT1 levels, protracts Kiss1 repression and delays puberty. This delay is mimicked by central pharmacological activation of SIRT1 or SIRT1 overexpression, achieved via transgenesis or virogenetic targeting to the ARC. Our results identify SIRT1-mediated inhibition of Kiss1 as key epigenetic mechanism by which nutritional cues and obesity influence mammalian puberty.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Vazquez MJ,Toro CA,Castellano JM,Ruiz-Pino F,Roa J,Beiroa D,Heras V,Velasco I,Dieguez C,Pinilla L,Gaytan F,Nogueiras R,Bosch MA,Rønnekleiv OK,Lomniczi A,Ojeda SR,Tena-Sempere Mdoi
10.1038/s41467-018-06459-9subject
Has Abstractpub_date
2018-10-10 00:00:00pages
4194issue
1issn
2041-1723pii
10.1038/s41467-018-06459-9journal_volume
9pub_type
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