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000291435 0247_ $$2doi$$a10.1038/s41588-024-01798-4
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000291435 037__ $$aDKFZ-2024-01405
000291435 041__ $$aEnglish
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000291435 1001_ $$00000-0002-5816-664X$$aKentistou, Katherine A$$b0
000291435 245__ $$aUnderstanding the genetic complexity of puberty timing across the allele frequency spectrum.
000291435 260__ $$aLondon$$bMacmillan Publishers Limited, part of Springer Nature$$c2024
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000291435 500__ $$a2024 Jul;56(7):1397-1411
000291435 520__ $$aPubertal timing varies considerably and is associated with later health outcomes. We performed multi-ancestry genetic analyses on ~800,000 women, identifying 1,080 signals for age at menarche. Collectively, these explained 11% of trait variance in an independent sample. Women at the top and bottom 1% of polygenic risk exhibited ~11 and ~14-fold higher risks of delayed and precocious puberty, respectively. We identified several genes harboring rare loss-of-function variants in ~200,000 women, including variants in ZNF483, which abolished the impact of polygenic risk. Variant-to-gene mapping approaches and mouse gonadotropin-releasing hormone neuron RNA sequencing implicated 665 genes, including an uncharacterized G-protein-coupled receptor, GPR83, which amplified the signaling of MC3R, a key nutritional sensor. Shared signals with menopause timing at genes involved in DNA damage response suggest that the ovarian reserve might signal centrally to trigger puberty. We also highlight body size-dependent and independent mechanisms that potentially link reproductive timing to later life disease.
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