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. 2017 Jun 29;7:4394. doi: 10.1038/s41598-017-03054-8

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Pedigrees of patients with clinically associated variants contributing to obesity Co-segregation of variants is shown where male (squares) and female (circles) family members consented to genotyping. Heterozygous (filled) and wild-type (empty) mutation carriers are indicated; in some cases, individuals were not available for genotyping (grey). Body mass index (BMI) (>27 kg/m² = overweight;>30 kg/m² = obesity) for adults and BMI standard deviation scores (BMI sds) for children are shown where data was available. (A) Obesity alone; (B) Obesity and Delay. MC4R mutations were excluded by prior Sanger sequencing of all individuals undergoing whole exome sequencing and the majority (1744/1811) of individuals undergoing targeted resequencing. The finding of four MC4R mutations in the remaining 82 individuals is in keeping with the prevalence of heterozygous MC4R mutations in this cohort as reported previously⁵.