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Experimental aspects of copy number variant assays at CCL3L1

Nature Medicine volume 15, pages 1115–1117 (2009)Cite this article

To the Editor:

Copy number variants (CNVs) are duplicated or deleted segments of the genome that vary in size from a few bases to several kilobases and comprise a substantial proportion of normal genomic variation1. The role of population-wide CNVs in disease has only recently come under investigation2,3. The gene encoding the chemokine (C-C) motif receptor CCR5, CCR5, on chromosome 3p21, has been associated with resistance to HIV-1 infection2. One of its ligands, CCL3L1, is encoded by a gene that lies in a CNV on chromosome 17q12 (ref. 4), which includes another CCR5 ligand, CCL4L1 (Supplementary Fig. 1), both of which have been reported to be associated with HIV-1/AIDS susceptibility2,5,6. CCR5 is associated with type 1 diabetes7, and hence we hypothesized that CCL3L1 is also associated with type 1 diabetes.

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Figure 1: Histograms of the frequency of the chromosome 17q12 CNV measure obtained using PRT and qPCR assays.

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Acknowledgements

This work was funded by the Juvenile Diabetes Research Foundation International, the Wellcome Trust and the UK National Institute for Health Research Cambridge Biomedical Research Center. The Cambridge Institute for Medical Research is in receipt of a Wellcome Trust Strategic Award (079895). We are grateful for the participation of the individuals with type 1 diabetes and the control individuals. We would like to thank the UK Medical Research Council and Wellcome Trust for funding the collection of DNA for the British 1958 Birth Cohort. DNA control samples were prepared and provided by S. Ring, R. Jones, M. Pembrey and W. McArdle (Avon Longitudinal Study of Pregnancy and Childhood Laboratory, Department of Social Medicine, University of Bristol), D. Strachan (Division of Community Health Sciences, St. George's, University of London) and P. Burton (Department of Genetics and Health Sciences (University of Leicester). Type 1 diabetes case DNA samples were prepared by K. Bourget, S. Duley, S. Hawkins, G. Coleman, M. Maisuria, S. Hood, E. King, T. Mistry, A. Simpson, S. Wood, S. Clayton, F. Wright and H. Stevens (Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge). Double scoring was performed by M. Hardy (Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge).

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Author notes

  1. Sarah F Field, Joanna M M Howson and Lisa M Maier: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Medical Genetics, Juvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK

    Sarah F Field, Joanna M M Howson, Neil M Walker, Deborah J Smyth, David G Clayton & John A Todd

  2. Division of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

    Lisa M Maier

  3. Program in Medical and Population Genetics, Broad Institute, Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts, USA

    Lisa M Maier

  4. Institute of Genetics and School of Biology, University of Nottingham, Queen's Medical Centre, Nottingham, UK

    Susan Walker & John A L Armour

Authors
  1. Sarah F Field
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Correspondence to John A Todd.

Supplementary information

Supplementary Figures, Supplementary Tables, Supplementary Methods, Supplementary Results and Supplementary Discussion

Supplementary Figures 1–2, Supplementary Tables 1–4, Supplementary Methods, Supplementary Results and Supplementary Discussion (PDF 404 kb)

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Field, S., Howson, J., Maier, L. et al. Experimental aspects of copy number variant assays at CCL3L1. Nat Med 15, 1115–1117 (2009). https://doi.org/10.1038/nm1009-1115

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