Authors

Ulrike Peters, Fred Hutchinson Cancer Center
Kari E. North, The University of North Carolina at Chapel Hill
Praveen Sethupathy, The University of North Carolina at Chapel Hill
Steve Buyske, Rutgers University–New Brunswick
Jeff Haessler, Fred Hutchinson Cancer Center
Shuo Jiao, Fred Hutchinson Cancer Center
Megan D. Fesinmeyer, Fred Hutchinson Cancer Center
Rebecca D. Jackson, The Ohio State University Wexner Medical Center
Lew H. Kuller, University of Pittsburgh Graduate School of Public Health
Aleksandar Rajkovic, University of Pittsburgh School of Medicine
Unhee Lim, University of Hawaiʻi Cancer Center
Iona Cheng, University of Pittsburgh School of Medicine
Fred Schumacher, USC Norris Comprehensive Cancer Center
Lynne Wilkens, University of Hawaiʻi Cancer Center
Rongling Li, National Human Genome Research Institute (NHGRI)
Keri Monda, The University of North Carolina at Chapel Hill
Georg Ehret, Johns Hopkins University School of Medicine
Khanh Dung H. Nguyen, Johns Hopkins University School of Medicine
Richard Cooper, Loyola University Chicago
Cora E. Lewis, UAB Department of Medicine
Mark Leppert, University of Utah School of Medicine
Marguerite R. Irvin, The University of Alabama at Birmingham
C. Charles Gu, Washington University in St. Louis
Denise Houston, Wake Forest University School of Medicine
Petra Buzkova, University of Washington
Marylyn Ritchie, Pennsylvania State University
Tara C. Matise, Rutgers University–New Brunswick
Loic Le Marchand, University of Hawaiʻi Cancer Center
Lucia A. Hindorff, National Human Genome Research Institute (NHGRI)
Dana C. Crawford, Vanderbilt University Medical Center
Christopher A. Haiman, USC Norris Comprehensive Cancer Center
Charles Kooperberg, Fred Hutchinson Cancer Center

Document Type

Article

Publication Date

1-1-2013

Abstract

Genetic variants in intron 1 of the fat mass- and obesity-associated (FTO) gene have been consistently associated with body mass index (BMI) in Europeans. However, follow-up studies in African Americans (AA) have shown no support for some of the most consistently BMI-associated FTO index single nucleotide polymorphisms (SNPs). This is most likely explained by different race-specific linkage disequilibrium (LD) patterns and lower correlation overall in AA, which provides the opportunity to fine-map this region and narrow in on the functional variant. To comprehensively explore the 16q12.2/FTO locus and to search for second independent signals in the broader region, we fine-mapped a 646-kb region, encompassing the large FTO gene and the flanking gene RPGRIP1L by investigating a total of 3,756 variants (1,529 genotyped and 2,227 imputed variants) in 20,488 AAs across five studies. We observed associations between BMI and variants in the known FTO intron 1 locus: the SNP with the most significant p-value, rs56137030 (8.3×10-6) had not been highlighted in previous studies. While rs56137030was correlated at r2>0.5 with 103 SNPs in Europeans (including the GWAS index SNPs), this number was reduced to 28 SNPs in AA. Among rs56137030 and the 28 correlated SNPs, six were located within candidate intronic regulatory elements, including rs1421085, for which we predicted allele-specific binding affinity for the transcription factor CUX1, which has recently been implicated in the regulation of FTO. We did not find strong evidence for a second independent signal in the broader region. In summary, this large fine-mapping study in AA has substantially reduced the number of common alleles that are likely to be functional candidates of the known FTO locus. Importantly our study demonstrated that comprehensive fine-mapping in AA provides a powerful approach to narrow in on the functional candidate(s) underlying the initial GWAS findings in European populations.

Publication Source (Journal or Book title)

PLoS Genetics

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