May 2006
Volume 47, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2006
Genomewide Scan in Amish Families Confirms Linkage of Ocular Refraction to Chromosome 1
Author Affiliations & Notes
  • R. Wojciechowski
    Genetic Epidemiology, Johns Hopkins School of Public Health, Baltimore, MD
    Inherited Disease Research Branch, NHGRI, Baltimore, MD
  • C. Moy
    Ophthalmology, University of Pennsylvania, Philadelphia, PA
  • G. Ibay
    Inherited Disease Research Branch, NHGRI, Baltimore, MD
  • E. Ciner
    Pennsylvania College of Optometry, Philadelphia, PA
  • J.E. Bailey–Wilson
    Inherited Disease Research Branch, NHGRI, Baltimore, MD
  • D. Stambolian
    Ophthalmology, University of Pennsylvania, Philadelphia, PA
  • Footnotes
    Commercial Relationships  R. Wojciechowski, None; C. Moy, None; G. Ibay, None; E. Ciner, None; J.E. Bailey–Wilson, None; D. Stambolian, None.
  • Footnotes
    Support  American Optometric Foundation CIBA Vision–Ezell Fellowship (RW); NEI grant EY12226 (DS); NHGRI(NIH) intramural program (RW, JEB–W, GI)
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 5819. doi:
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      R. Wojciechowski, C. Moy, G. Ibay, E. Ciner, J.E. Bailey–Wilson, D. Stambolian; Genomewide Scan in Amish Families Confirms Linkage of Ocular Refraction to Chromosome 1 . Invest. Ophthalmol. Vis. Sci. 2006;47(13):5819.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : The development of refractive error is mediated by environmental and genetic factors. We performed variance components (VC) and regression–based quantitative trait locus (QTL) linkage analyses on Old Order Amish families to identify genomic regions responsible for ocular refraction.

Methods: : We measured refraction on 454 individuals in 66 Old Order Amish families. Microsatellite genotyping with 387 polymorphic markers was performed on 348 individuals by the Center for Inherited Disease Research. The mean spherical equivalent refractive error in the sample population was –1.68D (SD=2.73), and 165 (47%) of the genotyped individuals had at least 1 D of myopia. QTL linkage analyses were performed on a logarithmic transformation of the mean refraction. We performed multipoint regression–based linkage analysis using the statistical package Merlin–regress assuming an underlying population mean refraction of 0 D, a variance of 10 and a heritability of 0.6. In addition, we combined the families into 14 extended pedigrees and performed VC analysis using the program SOLAR. Empirical p–values for VC analysis were assessed via simulation.

Results: : Regression–based QTL analysis yielded LOD score peaks of 1.2 (p=.01) and 1.5 (p=.004) on chromosome 1; and 3.2 (p=.00006) on chromosome 5. We also found suggestive evidence for linkage (i.e., LOD scores above 1) on chromosomes 7, 8, 13 and 14. VC analysis showed linkage peaks of 2.9 (p=.005) on chromosomes 1 and 3.0 (p=.003) on chromosome 13.

Conclusions: : These results provide evidence in support of a previously–identified QTL for ocular refraction on chromosome 1. We also identified several additional chromosomal regions that may harbor genes that mediate refractive development.

Keywords: refraction • linkage analysis • myopia 
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