Shared genetic aetiology of puberty timing between sexes and with health-related outcomes

Felix R. Day, Brendan Bulik-Sullivan, David A. Hinds, Hilary K. Finucane, Joanne M. Murabito, Joyce Y. Tung, Ken K. Ong and John R.B. Perry ()
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Felix R. Day: MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Box 285 Institute of Metabolic Science, Cambridge Biomedical Campus
Brendan Bulik-Sullivan: Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard
David A. Hinds: 23andMe Inc.
Hilary K. Finucane: Harvard School of Public Health
Joanne M. Murabito: NHLBI’s and Boston University’s Framingham Heart Study
Joyce Y. Tung: 23andMe Inc.
Ken K. Ong: MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Box 285 Institute of Metabolic Science, Cambridge Biomedical Campus
John R.B. Perry: MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Box 285 Institute of Metabolic Science, Cambridge Biomedical Campus

Nature Communications, 2015, vol. 6, issue 1, 1-6

Abstract: Abstract Understanding of the genetic regulation of puberty timing has come largely from studies of rare disorders and population-based studies in women. Here, we report the largest genomic analysis for puberty timing in 55,871 men, based on recalled age at voice breaking. Analysis across all genomic variants reveals strong genetic correlation (0.74, P=2.7 × 10−70) between male and female puberty timing. However, some loci show sex-divergent effects, including directionally opposite effects between sexes at the SIM1/MCHR2 locus (Pheterogeneity=1.6 × 10−12). We find five novel loci for puberty timing (P

Date: 2015
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DOI: 10.1038/ncomms9842

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