Polycomb represses a gene network controlling puberty via modulation of histone demethylase Kdm6b expression

Hollis Wright, Carlos F. Aylwin, Carlos A. Toro, Sergio R. Ojeda, Alejandro Lomniczi

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Female puberty is subject to Polycomb Group (PcG)-dependent transcriptional repression. Kiss1, a puberty-activating gene, is a key target of this silencing mechanism. Using a gain-of-function approach and a systems biology strategy we now show that EED, an essential PcG component, acts in the arcuate nucleus of the hypothalamus to alter the functional organization of a gene network involved in the stimulatory control of puberty. A central node of this network is Kdm6b, which encodes an enzyme that erases the PcG-dependent histone modification H3K27me3. Kiss1 is a first neighbor in the network; genes encoding glutamatergic receptors and potassium channels are second neighbors. By repressing Kdm6b expression, EED increases H3K27me3 abundance at these gene promoters, reducing gene expression throughout a gene network controlling puberty activation. These results indicate that Kdm6b repression is a basic mechanism used by PcG to modulate the biological output of puberty-activating gene networks.

    Original languageEnglish (US)
    Article number1996
    JournalScientific Reports
    Volume11
    Issue number1
    DOIs
    StatePublished - Dec 2021

    ASJC Scopus subject areas

    • General

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